Review Sheet 15 Spinal Cord and Spinal Nerves

• Periodical List
• Front Oncol
• PMC7026187

Front Oncol. 2020; 10: 99.

Intracranial Metastases Originating From Pediatric Primary Spinal Cord Glioblastoma Multiforme: A Case Report and Literature Review

Dengpan Song

¹Department of Neurosurgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China

Dingkang Xu

¹Department of Neurosurgery, The Outset Affiliated Hospital of Zhengzhou University, Zhengzhou, China

Qiang Gao

^aneDepartment of Neurosurgery, The Kickoff Affiliated Hospital of Zhengzhou University, Zhengzhou, China

Peizhu Hu

²Section of Pathology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Cathay

Fuyou Guo

¹Department of Neurosurgery, The Commencement Affiliated Infirmary of Zhengzhou University, Zhengzhou, China

Received 2019 Oct 15; Accepted 2020 Jan 20.

Abstract

Main spinal string glioblastoma multiforme (scGBM) is an uncommon entity in pediatrics, and intracranial metastasis originating in spinal string gliomas is very rare. A 7-year-old female presented with weakness in the limbs, paralysis of the lower limbs and incontinence. The initial MRI of the spinal cord revealed expansion and abnormal signals from T2 to T5. She was initially diagnosed with Neuromyelitis optica spectrum disorders and treated with high-dose glucocorticoid and gamma globulin. Four months afterwards, her symptoms worsened and follow-upward imaging showed multiple intracranial mass lesions. We performed a subtotal resection of the right thalamic basal ganglia tumor and gross total resection of the right frontal lobe tumor nether microscopic exam. Histopathology revealed scGBM with intracranial metastasis and the molecular pathology diagnosis suggested H3K27M mutant diffuse midline glioma WHO grade IV, which had previously been misdiagnosed every bit a Neuromyelitis optica spectrum disorders. We review the literature of intracranial metastases originating from pediatric main spinal cord glioblastoma multiforme and summarize possible methods of differentiation, including changes in musculus strength or tone, intramedullary heterogeneously enhancing solitary mass lesions and cord expansion in MRI. Finally, we emphasize that in unexpected radiological changes or disadvantageous response to the handling, a biopsy to attain a pathological diagnosis is necessary to discard other diseases, especially neoplasms.

Keywords: spinal cord glioblastoma, intracranial metastases, pediatric, case written report, literature review

Introduction

Glioblastoma multiforme (GBM) is the most common primary CNS tumor in adults but information technology is not common in children. Nevertheless, among the group of cancerous glial tumors, high grade glioma is the most frequent diagnosis in children. Furthermore, the incidence of intramedullary tumors is very rare in children; most are depression form gliomas (1). A spinal cord origin of glioblastoma in both adults and children is rare (ii). Metastatic intracranial GBM disseminating from a primary intramedullary spinal GBM is extremely uncommon and has rarely been reported in the earth literature. Here, we review the literature (three–20) on intracranial metastases originating from main scGBM in pediatric patients (Tabular array 1). Surgical resection followed past radiotherapy and concomitant adjuvant chemotherapy is the recommended treatment in children.

Tabular array one

Review of the literature on intracranial metastases originating from primary spinal string glioblastoma multiforme in pediatric patients.

Example no.	References	Age(years)/Sex	Level of tumor	Surgery	RT	CT	Survival (mos)
ane	O'connell et al. (17)	xvi/1000	Conus	Biopsy	Y	N	16
2	Tashiro et al. (xvi)	12/F	Conus	STR	Northward	N	eleven
three	Johnson et al. (15)	8/F	T11-L3	STR	Y	Y	fourteen
iv	Cohen et al. (20)	17/F	Thoracic	NR	Y	NR	x
5		16/F	Conus	NR	Y	NR	6
six		14/Grand	Conus	NR	Y	NR	four
vii		10/F	Cervical	NR	Y	NR	5
viii		ix/M	Cervical	NR	Y	NR	1
9	Allen et al. (14)	4/M	Holocord	STR	N	Y	37
10		v/M	Thoracic	Biopsy	Y	Y	68
11		15/M	Cervical	STR	Y	Y	48
12	Klepstad et al. (19)	12/F	Cervical	STR	NR	NR	ii
13	Kawashima et al. (13)	8/F	C7-T11	Surgery	Y	Y	12
14	Caroli et al. (12)	6/M	T9-T11	STR	Y	Y	nine
15	Stecco et al. (xi)	14/Thousand	Conus	STR	Due north	Northward	10
16	Battaglia et al. (9)	eleven/One thousand	T4-T5	GTR	Y	Y	6
17	Bonde et al. (10)	16/G	Conus	GTR	Y	Due north	6
eighteen	Sun et al. (8)	14/One thousand	Conus	STR	N	North	xvi
19	Kim et al. (18)	16/F	T12-L1	Biopsy	Y	Y	12
twenty	Mori et al. (seven)	10/F	Conus	Biopsy	Y	Y	14
21	Derinkuyu et al. (six)	nine/F	T8-T10	Surgery	Y	Y	8
22	Kokkalis et al. (5)	12/One thousand	T4-T8	GTR	Y	Y	20
23	Kumar et al. (3)	4/M	Cervicothoracic	Biopsy	Y	Y	4
24	Yan et al. (4)	10/K	T11-L1	GTR	Y	Y	14
25	The present instance	7/F	T2-T5	STR	North	Due north	1

NR, non reported. The information were obtained from PubMed.

This study presents an uncommon case of scGBM with intracranial metastasis closely mimicking Neuromyelitis optica spectrum disorders in both symptoms and MRI findings. The unique features of MRI and the clinical symptoms are summarized in the nowadays article.

Instance Study

A 7-year-sometime female person patient was admitted to the hospital because of a 7-days history of weakness in her left lower limb, intermittent breast pain, and bedevilment at dark. The patient presented with a fever of more than 39 degrees centigrade, urinary and fecal incontinence and bilateral limb paralysis afterwards 16 days, and her temperature was normal after loftier-dose glucocorticoid and gamma globulin intensive therapy, due to the suspicion of acute transverse myelitis. Gamma globulin (two g/kg) and methyl prednisolone (20 mg/kg) were administered for 4 days. She underwent lumbar puncture, and a cerebrospinal fluid (CSF) assay showed that the protein level was 4073.4 mg/l. Then, her symptoms deteriorated in her upper limbs, and the patient had a seizure. Imaging examinations and urine culture analysis confirmed a diagnosis of pneumonia and urinary tract infection. She received meropenems and cephalosporins, but the neurological symptoms did not amend. So, because the mild remission from the initial intensive therapy, gamma globulin (2 k/kg) and methyl prednisolone (20 mg/kg) were administered once again 5 days subsequently. The CSF examination showed a growing CD19-positive T and B cell count (815 U/L). She was diagnosed with a Neuromyelitis optica spectrum disorder and was treated with gamma globulin (two k/kg) on day 10 and Rituximab 0.iii mg on day 15. Her spinal cord and brain MRI findings revealed changes in accordance with the course and severity of the disease (Figures 1, ​ 2).

An early MRI examination showed expansion and aberrant signals from T2 to T5 (A,B). Seven days afterward, a spinal MRI showed the lesions had become enlarged (C,D). A follow-up MRI showed multiple aberrant signals in the cervicothoracic spinal cord, and the T1 to T6 level spinal cord was enlarged and showed a long T2 signal (East,F). The aberrant point range and the thickening of T1 to T6 level crista medulla had slightly decreased (Thousand). One month later, the abnormal expanse of the point was enlarged, and the betoken was enhanced (H). In a postoperative spinal contrast enhanced MRI, there were multiple signals showing heterogeneous enhancement in the medulla oblongata, the c3-7 level cervical spinal string and its margin, the t3-6 level spinal canal, and the t2-l1 level spinal cord and its margin. Patchy enhancement was observed in the soft tissue behind the thoracolumbar vertebrae, the bilateral cerebellum, the inductive pontine cistern and the fourth ventricle (I).

An early on MRI showed that the brain parenchyma was normal (A–C). Over 2 weeks later, an MRI showed that the right occipital lobe, bilateral parietal lobe, right thalamus, correct hippocampus and temporal lobe showed a canvass equal signal on T1 and a long signal on T2 (D,East). Preoperatively, on a brain MRI exam, abnormal signals were plant in bilateral cerebellum, inductive cistern of pons, correct cerebellopontine angle, fourth ventricle, bilateral hippocampus, right basal ganglia, bilateral paraventricles, right frontal lobe, left temporal parietal lobe, pineal region, left thalamus, and left cerebral peduncle (F).

The patient presented to our establishment with a 4-months history of weakness in her limbs. Her physical examinations showed bilateral lower limb muscular tension with an Ashworth Class of one; right and left upper limb musculus strength with grades of 4/5 and three/5, respectively; bilateral lower limb muscle strength with a form of 0/five; hypesthesia of superficial sense below C2 (mainly in the left limbs); not-cooperation on a deep sense examination; hyperfunctional bilateral biceps and triceps tendon reflexes (++); a hyperfunctional bilateral patellar and Achilles tendon reflexes (+++) with a grade of 3/4; a bilateral ankle clonus (+); and a positive bilateral Babinski'south sign (+), which was suggestive of encephalon involvement. A brain contrast-enhanced MRI examination showed multiple intracranial lesions (Effigy ii).

We suspected a high-form glioma and performed subtotal resection of the right thalamic basal ganglia tumor and gross total resection of the correct frontal lobe tumor nether microscopic examination. The pathological diagnosis was WHO form IV GBM, and the molecular pathology diagnosis was H3K27M mutant diffuse midline glioma WHO grade IV (Figure iii).

The histopathology of correct basal nodule and frontal lobe indicating a malignant tumor (A,B). By immunohistochemistry, the tumor cells were positive for GFAP (C), S-100 protein (K), Oligo-2, ATRX (E), P53 (H), SOX-10, Syn, CD56, and INI-1 and negative for IDH-1 (F), NeuN and H3K27me3 (D). Moreover, they were weakly positive for CD99, and threescore% of them were positive for Ki-67 (I). The final diagnosis was WHO course IV glioblastoma (GBM), and the molecular pathology diagnosis was H3K27M mutant diffuse midline glioma WHO grade IV.

Postoperatively, the patient was treated with antiepileptic drugs and neurotrophic drugs, such every bit injection of mouse nerve growth factor. On a postoperative spinal MRI, there were multiple signals showing heterogeneous enhancement in the medulla oblongata, at the c3-vii level of the cervical spinal cord and margin, at the t3-6 level of the spinal canal, and at the t2-l1 level of the spinal cord and its margin. Patchy enhancement was observed in the soft tissue behind the thoracolumbar vertebrae, the bilateral cerebellum, the anterior pontine cistern and the fourth ventricle.

Eleven days later the operation, the patient developed status epilepticus and coma. Despite conservative treatment, her full general condition and neurological status did non amend. Her relatives asked that she be discharged two days afterwards, and she died a month later.

Discussion

High-grade gliomas (HGGs) are the most common group of pediatric malignant CNS neoplasms, and midline tumor location in children is more frequent than in adults (21). As far as principal spinal glioblastoma, Beyer et al. found that information technology mainly touch on younger patients, and the median age at diagnosis in their cohort was 22 years (2). Yet, the incidence of chief spinal string glioblastoma multiforme (scGBM) in the pediatric age group is still very rare (22). The most common pattern of progressive disease is local recurrence, and intracranial metastasis of spinal cord gliomas is extremely rare (21). Here, nosotros review the literature (3–20) on intracranial metastases originating from primary scGBM in pediatric patients (Table 1). Fifty-six percent of the children were male person and 44% were female. The median OS was 10 months. 30-two percent of the tumors were conus, 28% were thoracic, sixteen% were cervical, 12% were thoracolumbar, 8% were cervicothracic, and 4% were at a holocord location. Regarding surgery type, subtotal resection was performed in 36% of the cases, and biopsy was achieved in 20%. GTR was performed in sixteen% of the cases and 8% mentioned merely surgery. Regarding treatment type, 20% of the children underwent surgery simply. Forty-viii percent received both RT and CT after surgery, 28% received only RT after surgery, and 4% received only CT subsequently surgery. Several factors are associated with the tendency of a tumor to disseminate; these include a immature historic period, a high histology grade, cellular anaplasia, oligodendroglial differentiation, overexpression of epidermal growth factor receptor, increasing Ki-67 values and immunosuppressed states (23–25), some of which were found in our case. Intracranial seeding of spinal string glioma may occur due to dissemination of the tumor into the spinal subarachnoid space and subsequent intracranial spread into the cerebral subarachnoid space or brain parenchyma via the CSF (26, 27). Hence, we believe that information technology is necessary to perform cytologic examinations of the CSF so that the metastasis can exist discovered before, fifty-fifty when no associated abnormal CSF is plant, as occurred in our case.

MRI is an essential auxiliary diagnostic method that helps when judging the location of a spinal tumor and is very useful and helpful for tumor differentiation. The patient's tumors always showed mixed hypo-isointense signals on T1-weighted images (T1WI) and hyperisointense signals on T2-weighted images (T2WI). On MRI with contrast, scGBM presents with an irregular zone of contrast enhancement, and could be expressed every bit intramedullary heterogeneously enhancing solitary mass lesions and string expansion in children (28). With the development of the disease, this operation will become more obvious, and in that location may exist local or diffuse metastasis. The majority of intramedullary tumors in children are astrocytomas and ependymomas (29), with ependymomas characterized past a high incidence of syringomyelia and homogeneously enhanced solid tumor sections. Low-form astrocytoma usually lacks pregnant reinforcement after Gd-DTPA is applied. However, because of the imaging non-specificity and rarity of scGBM, it is difficult to diagnose this type of lesion based on MRI lonely. It tin mimic an epidural pathology, in some cases including an epidural abscess (30), Neuromyelitis optica spectrum disorders or lymphoma on contrast MRI. Therefore, in the case of some special spinal cord diseases that are difficult to recognize based on clinical and imaging findings, a biopsy and pathological examination should be performed to avert misdiagnosis.

Spinal GBM is identified based on pathology parameters, such equally its intracranial counterparts, including nuclear atypia, mitotic activity, vascular proliferation, and necrosis (28, 30), every bit well as immunohistochemical parameters, such equally GFAP and S-100 positivity with a loftier Ki-67 leveling alphabetize (28, 31), the latter of which was observed in the intracranial lesions in our example. While the histology of HGGs between adults and children appears identical, the biology of the tumors may vary significantly. The mutation rate of P53 in children with GBM was 40%. Overexpression of p53 was significantly associated with dramatically reduced progression-gratuitous survival (PFS) at v years, while mutations in TP53 were non-significantly associated with adverse prognosis (32). Mutations of IDH-fifty and IDH-ii accept a low incidence in primary GBM, and high-course glioma (HGG) with IDH gene mutation has a significantly improve prognosis (33). The promoter methylation charge per unit of MGMT was 40–57% in GBM, and the methylation of the MGMT promoter suggests that the prognosis of patients with GBM is better in both adults and children, while GBM with MGMT promoter methylation may exist sensitive to alkylating agent (32, 34). Simply five.0% of cases of glioblastoma multiforme were associated with 1p/19q codeletion, and Clark et al. (35) confirmed that 1p/19q testing is not useful on gliomas that are histologically GBM. A full of 15.3% of enrolled GBM cases demonstrated loss of ATRX expression (ATRX-), and the developed patients with ATRX- showed better survival than patients with analogue proteins expressed in GBM (36). In addition, H3K27me3 was negative in molecular pathology, suggesting that H3K27M mutation may be present; thus, the final molecular pathology diagnosis may exist H3K27M mutant diffuse midline glioma WHO grade Iv. The diagnosis of WHO grade Four GBM is mainly based on routine histopathology. Overall survival was significantly shorter when the H3K27M mutation was present in HGG, and HGG patients positive for the H3K27M mutation are more than three times more susceptible to succumbing to this affliction past more than ii years, compared to patients negative for the mutation (37). Therefore, the presence of H3K27M mutation may suggest H3K27M mutant diffuse midline glioma and indicate a high metastasis rate and poor prognosis.

Surgery is still the chief treatment for spinal GBM and related intracranial metastasis. However, in that location is controversy regarding the surgical extent of resection that should exist achieved in loftier-grade spinal glioma patients. Ononiwu et al. (38) noted that children treated with GTR survived longer on boilerplate than those treated with STR. However, Konar et al. (22) establish that extent of resection does non have a direct relationship with OS. Moreover, the surgical procedure should also exist selected in consideration of the preservation of neural part. In some cases of tardily-stage scGBM, the tumor is too close to the functional nervus area to exist separated completely, and in these cases, fractional resection should be performed while preserving the original nervus function. We believe that total resection should not exist performed solely to foreclose recurrence but that quality of life should likewise exist improved and survival time maximized, both of which tin be accomplished by precise subtotal resection with preservation of neural function. In the example presented here, to remove as many tumors as possible without compromising safe and meliorate the quality of life of patient, we performed a full microscopic resection of the right frontal lobe tumor and extended the resection to the glial hyperplasia zone. Nevertheless, the right thalamic basal ganglia tumor was resected only subtotally to avoid serious dysfunction due to its ill-defined boundary and infiltration of conduction tracts.

The function of radiotherapy and chemotherapy in GBM is still much debated. In their study of 158 high-class spinal cord gliomas, Jiang Lui et al. (39) found that the use of postoperative RT offered a survival benefit, peculiarly in pediatrics (22). Minehan et al. (40) found that postoperative RT essentially enhanced overall survival in high grade gliomas. However, Lam et al. (41) found that increased RT for spinal GBM does not prolong Bone in pediatrics. Similarly, reports well-nigh the furnishings of chemotherapy have produced conflicting results. Some reviews have non demonstrated a significant difference in long-term survival between groups treated with or without temozolomide (TMZ) (42). All the same, some studies have found that the TMZ improved prognoses in both adults and children (22, 43). With regard for radiotherapy, we do not advise that it may cause a deterioration in medullary function, edema and reduced quality of life. In addition, cistron-based detection and molecular targeted therapy may as well play a role in GBM (44).

Neuromyelitis optica spectrum disorders (NMOSDs) are rare autoimmune diseases in which NMO-IgG selectively binds to aquaporin-4 (AQP4). NMOSDs mainly involves the optic nerve, spinal cord and central nervous organization in the form of an inflammatory response in these areas. According to the new NMOSD diagnostic criteria, we suggest some characteristics that may be used to differentiate them: (1) serum AQP4 antibiotic detection; (2) association with clinical symptoms and MRI findings typical of optic neuritis; (three) in NMOSD, few muscles are involved, while scGBM oft manifests with changes in muscle strength or tone, such every bit progressive weakness or paresthesia in both lower limbs; (four) a fast-moving process is oft observed in NMOSD; and (5) rapid and significant improvement after high-dose glucocorticoid handling. Nevertheless, due to similarities in clinical symptoms and imaging findings and the rarity of both diseases, we were unable to accurately differentiate scGBM and NMOSD. There were some major potential contributors to the misdiagnosis that occurred in our case: (1) the nonspecific presentation of symptoms and imaging findings, (2) the rapid progression of the disease over time, and (3) the slight improvement observed after glucocorticoid treatment. This improvement may have been due to the remission of the secondary inflammation of the tumor rather than the treatment for NMOSD. There are very few records of scGBM imitating NMOSD. Nosotros emphasize the necessity of biopsy or surgical pathology in differentiating between spinal string inflammation and neoplastic disease.

While acute transverse myelitis (ATM) is a relatively common disease, it is rare in children. Compared with scGBM, ATM may nowadays with essentially higher protein levels in CSF (mean value of 17,375 g/dL and range 45–ane,120 thou/dL) and a notable absence of T1 hypointensity on spinal MRI (45), but these are non diagnostic. Because the imaging findings of ATM are always relatively variable and not-specific, MRI plays simply a differential role in some typical cases. In the present example, a rise in the CSF protein level and slight improvement in the patient'south condition were observed, and these may have been influenced by the secondary inflammation of the tumor, affecting the doctor'due south diagnosis and causing the misdiagnosis. Therefore, it is crucial to perform surgical biopsy or surgical pathology in indistinguishable cases.

Primary key nervous system lymphoma (PCNSL) is a rare aggressive non-Hodgkin lymphoma confined to the encephalon, spine, eyes, and leptomeninges. It represents only four% of intracranial neoplasms, and iv–half dozen% of extranodal lymphomas. Phenotypically, PCNSL is nearly ever a diffuse large B-cell lymphoma (DLBCL) (46). This disease is very rare in pediatric patients, and its clinical features and treatment outcomes in this group are not well-understood. (47). Primary CNS lymphoma is almost non-real in pediatric-aged patients and should not be taken into account in the differential diagnosis in such cases.

Conclusion

Intracranial metastases originating from pediatric primary scGBM are extremely rare, and their atypical symptoms and imaging findings are the main causes of their misdiagnosis every bit other weather, such every bit NMOSD, ATM, or lymphoma. Therefore, we should fully consider the possibility of scGBM and pay attention to differential diagnoses. If a patient's clinical symptoms and MRI and other auxiliary examinations exercise not let a definitive diagnosis, it is necessary to perform a biopsy or surgical pathology every bit shortly as possible.

Data Availability Argument

All datasets generated for this written report are included in the article/supplementary material.

Ethics Statement

The protocol was approved by the medical ethical committee of Zhengzhou University. This patient's parents gave written informed consent. The authors affirm that written informed consent was obtained from the participant for the publication of this case report.

Author Contributions

DS: manuscript writing. DX: conception and critical review. QG and PH: image extraction and pathological review. FG: conception and disquisitional review. All authors proofread and approved the manuscript.

Disharmonize of Involvement

The authors declare that the research was conducted in the absence of whatsoever commercial or financial relationships that could be construed as a potential conflict of interest.

Acknowledgments

The authors thank the members of their enquiry group for useful discussions.

References

one. Ostrom QT, Cioffi 1000, Gittleman H, Patil N, Waite K, Kruchko C, et al. . CBTRUS statistical study: main brain and other primal nervous system tumors diagnosed in the United States in 2012-2016. Neuro Oncol. (2019) 21(Suppl. 5):v1-v100. ten.1093/neuonc/noz150 [PMC gratuitous article] [PubMed] [CrossRef] [Google Scholar]

2. Beyer S, von Bueren AO, Klautke 1000, Guckenberger M, Kortmann RD, Pietschmann Southward, et al. . A systematic review on the characteristics, treatments and outcomes of the patients with master spinal glioblastomas or gliosarcomas reported in literature until march 2015. PLoS ONE. (2016) xi:e0148312. 10.1371/journal.pone.0148312 [PMC gratis article] [PubMed] [CrossRef] [Google Scholar]

3. Kumar A, Rashid South, Singh S, Li R, Dure LS. Spinal cord diffuse midline glioma in a 4-year-old male child. Child Neurology Open. (2019) half-dozen:2329048X1984245. 10.1177/2329048X19842451 [PMC gratuitous commodity] [PubMed] [CrossRef] [Google Scholar]

4. Yan C, Kong X, Yin H, Wang Y, He H, Zhang H, et al. . Glioblastoma multiforme in conus medullaris with intracranial metastasis afterwards postoperative adjuvant therapy. Medicine. (2017) 96:e6500. x.1097/MD.0000000000006500 [PMC free article] [PubMed] [CrossRef] [Google Scholar]

v. Kokkalis P, Chamilos C, Sgouros S. Primary spinal glioblastoma multiforme with cognitive parenchymal metastasis in a child. Pediatr Neurosurg. (2016) 51:325–6. 10.1159/000446401 [PubMed] [CrossRef] [Google Scholar]

6. Derinkuyu BE, Boyunaga O, Okur A, Alimli AG, Oztunali C, Damar C, et al. . Primary intraspinal glioblastoma multiforme in a child. Spine J. (2015) 15:e37–viii. 10.1016/j.spinee.2015.07.451 [PubMed] [CrossRef] [Google Scholar]

7. Mori K, Imai S, Shimizu J, Taga T, Ishida M, Matsusue Y. Spinal glioblastoma multiforme of the conus medullaris with holocordal and intracranial spread in a child: a case report and review of the literature. Spine J. (2012) 12:e1–6. ten.1016/j.spinee.2011.12.005 [PubMed] [CrossRef] [Google Scholar]

8. Sun J, Wang Z, Li Z, Liu B. Microsurgical treatment and functional outcomes of multi-segment intramedullary spinal cord tumors. J Clin Neurosci. (2009) 16:666–71. 10.1016/j.jocn.2008.08.016 [PubMed] [CrossRef] [Google Scholar]

9. Battaglia S, Albini Riccioli L, Bartiromo F, Galassi Due east, Marliani AF, Leonardi 1000. Childhood spinal glioblastoma multiforme with intracranial dissemination: a instance report. Neuroradiol J. (2007) 20:500–4. 10.1177/197140090702000504 [PubMed] [CrossRef] [Google Scholar]

10. Bonde V, Balasubramaniam Southward, Goel A. Glioblastoma multiforme of the conus medullaris with holocordal spread. J Clin Neurosci. (2007) 15:601–3. 10.1016/j.jocn.2006.12.015 [PubMed] [CrossRef] [Google Scholar]

11. Stecco A, Quirico C, Giampietro A, Sessa G, Boldorini R, Carriero A. Glioblastoma multiforme of the conus medullaris in a child: description of a case and literature review. AJNR Am J Neuroradiol. (2005) 26:2157–60. [PMC free commodity] [PubMed] [Google Scholar]

12. Caroli Eastward, Salvati M, Ferrante L. Spinal glioblastoma with brain relapse in a child: clinical considerations. Spinal Cord. (2005) 43:565–7. 10.1038/sj.sc.3101749 [PubMed] [CrossRef] [Google Scholar]

xiii. Kawashima A, Sasajima T, Sugawara T, Takahashi M, Suzuki A, Higashiyama North, et al. . [Unusual MR appearance of intracranial dissemination from cervical glioblastoma]. No Shinkei Geka. (2004) 32:937–44. [PubMed] [Google Scholar]

14. Allen JC, Aviner Southward, Yates AJ, Boyett JM, Cherlow JM, Turski PA, et al. . Treatment of high-form spinal string astrocytoma of childhood with "eight-in-1" chemotherapy and radiotherapy: a pilot study of CCG-945. Children's Cancer Group. J Neurosurg. (1998) 88:215–twenty. 10.3171/jns.1998.88.2.0215 [PubMed] [CrossRef] [Google Scholar]

fifteen. Johnson DL, Schwarz S. Intracranial metastases from cancerous spinal-cord astrocytoma. Case written report. J Neurosurg. (1987) 66:621–five. 10.3171/jns.1987.66.4.0621 [PubMed] [CrossRef] [Google Scholar]

sixteen. Tashiro Yard, Tachibana S, Tsura One thousand. [Clinicopathological studies of spinal string neoplasm with disseminating intracranial metastasis perchance producing akinetics mutism]. No To Shinkei. (1976) 28:1311–8. [PubMed] [Google Scholar]

17. O'connell JE. The subarachnoid dissemination of spinal tumours. J Neurol Neurosurg Psychiatry. (1946) 9:55–62. 10.1136/jnnp.9.2.55 [PMC free article] [PubMed] [CrossRef] [Google Scholar]

xviii. Kim WH, Yoon SH, Kim CY, Kim KJ, Lee MM, Choe G, et al. . Temozolomide for cancerous principal spinal string glioma: an feel of six cases and a literature review. J Neuro-Oncol. (2011) 101:247–54. 10.1007/s11060-010-0249-y [PubMed] [CrossRef] [Google Scholar]

nineteen. Klepstad P, Borchgrevink P, Hval B, Flaat Due south, Kaasa S. Long-term treatment with ketamine in a 12-yr-one-time girl with severe neuropathic hurting acquired past a cervical spinal tumor. J Pediatr Hematol Oncol. (2001) 23:616–ix. 10.1097/00043426-200112000-00013 [PubMed] [CrossRef] [Google Scholar]

20. Cohen AR, Wisoff JH, Allen JC, Epstein F. Malignant astrocytomas of the spinal cord. J Neurosurg. (1989) lxx:l–four. x.3171/jns.1989.lxx.i.0050 [PubMed] [CrossRef] [Google Scholar]

21. Grill J, Massimino M, Bouffet E, Azizi AA, McCowage G, Cañete A, et al. . Phase 2, open-label, randomized, multicenter trial (HERBY) of bevacizumab in pediatric patients with newly diagnosed high-class glioma. J Clin Oncol. (2018) 36:951–8. 10.1200/JCO.2017.76.0611 [PubMed] [CrossRef] [Google Scholar]

22. Konar SK, Bir SC, Maiti TK, Nanda A. A systematic review of overall survival in pediatric principal glioblastoma multiforme of the spinal cord. J Neurosurg Pediatr. (2017) 19:239–48. x.3171/2016.8.PEDS1631 [PubMed] [CrossRef] [Google Scholar]

23. Faria MH, Gonçalves BP, do Patrocínio RM, de Moraes-Filho MO, Rabenhorst SH. Expression of Ki-67, topoisomerase IIalpha and c-MYC in astrocytic tumors: correlation with the histopathological grade and proliferative status. Neuropathology. (2006) 26:519–27. 10.1111/j.1440-1789.2006.00724.x [PubMed] [CrossRef] [Google Scholar]

24. Penar PL, Khoshyomn Southward, Bhushan A, Tritton TR. Inhibition of epidermal growth gene receptor-associated tyrosine kinase blocks glioblastoma invasion of the brain. Neurosurgery. (1997) forty:141–51. 10.1097/00006123-199701000-00032 [PubMed] [CrossRef] [Google Scholar]

25. Eade OE, Urich H, Metastasising gliomas in immature subjects J Pathol. (1971) 103:245–56. 10.1002/path.1711030407 [PubMed] [CrossRef] [Google Scholar]

26. Jeong SM, Chung YG, Lee JB, Shin IY. Intracranial broadcasting from spinal cord anaplastic astrocytoma. J Kor Neurosurg Soc. (2010) 47:68. 10.3340/jkns.2010.47.one.68 [PMC costless article] [PubMed] [CrossRef] [Google Scholar]

27. Figueiredo EG, Matushita H, Machado AG, Plese JP, Rosemberg S, Marino R. Leptomeningeal dissemination of pilocytic astrocytoma at diagnosis in childhood: ii cases report. Arq Neuropsiquiatr. (2003) 61:842–seven. 10.1590/S0004-282X2003000500025 [PubMed] [CrossRef] [Google Scholar]

28. Lober R, Sharma Due south, Bell B, Free A, Figueroa R, Sheils CW, et al. . Pediatric primary intramedullary spinal cord glioblastoma. Rare Tumors. (2010) 2:e48. x.4081/rt.2010.e48 [PMC free commodity] [PubMed] [CrossRef] [Google Scholar]

29. Winograd E, Pencovich N, Yalon 1000, Soffer D, Beni-Adani L, Constantini S. Malignant transformation in pediatric spinal intramedullary tumors: example-based update. Childs Nerv Syst. (2012) 28:1679–86. 10.1007/s00381-012-1851-4 [PubMed] [CrossRef] [Google Scholar]

30. Marciano R, Ahammad Z, Awuor V. Thoracic spinal cord glioblastoma mimicking epidural abscess: case report and literature review. Cureus. (2017) 9:e1631. 10.7759/cureus.1631 [PMC free article] [PubMed] [CrossRef] [Google Scholar]

31. Purkayastha A, Sharma N, Sridhar MS, Abhishek D. Intramedullary glioblastoma multiforme of spine with intracranial supratentorial metastasis: progressive illness with a multifocal pic. Asian J Neurosurg. (2018) thirteen:1209–12. 10.4103/ajns.AJNS_67_17 [PMC gratis article] [PubMed] [CrossRef] [Google Scholar]

32. MacDonald TJ, Aguilera D, Kramm CM, Treatment of high-grade glioma in children and adolescents . Neuro-Oncology. (2011) 13:1049–58. 10.1093/neuonc/nor092 [PMC free commodity] [PubMed] [CrossRef] [Google Scholar]

33. Yan H, Parsons DW, Jin Thousand, McLendon R, Rasheed BA, Yuan W, et al. . IDH1 and IDH2 mutations in gliomas. N Engl J Med. (2009) 360:765–73. 10.1016/S0513-5117(09)79085-four [PMC free commodity] [PubMed] [CrossRef] [Google Scholar]

34. Bleeker Atomic number 26, Molenaar RJ, Leenstra S. Recent advances in the molecular understanding of glioblastoma. J Neuro-Oncol. (2012) 108:11–27. 10.1007/s11060-011-0793-0 [PMC free article] [PubMed] [CrossRef] [Google Scholar]

35. Clark KH, Villano JL, Nikiforova MN, Hamilton RL, Horbinski C. 1p/19q testing has no significance in the workup of glioblastomas. Neuropathol Appl Neurobiol. (2013) 39:706–17. 10.1111/nan.12031 [PMC gratuitous article] [PubMed] [CrossRef] [Google Scholar]

36. Chaurasia A, Park SH, Seo JW, Park CK. Immunohistochemical analysis of ATRX, IDH1 and p53 in glioblastoma and their correlations with patient survival. J Korean Med Sci. (2016) 31:1208. 10.3346/jkms.2016.31.8.1208 [PMC gratuitous article] [PubMed] [CrossRef] [Google Scholar]

37. Lu VM, Alvi MA, McDonald KL, Daniels DJ. Impact of the H3K27M mutation on survival in pediatric high-grade glioma: a systematic review and meta-assay. J Neurosurg Pediatr. (2019) 23:308–xvi. 10.3171/2018.9.PEDS18419 [PubMed] [CrossRef] [Google Scholar]

38. Ononiwu C, Mehta V, Bettegowda C, Jallo G. Pediatric spinal glioblastoma multiforme: electric current treatment strategies and possible predictors of survival. Childs Nerv Syst. (2012) 28:715–20. ten.1007/s00381-012-1705-0 [PubMed] [CrossRef] [Google Scholar]

39. Liu J, Zheng Chiliad, Yang Due west, Lo SL, Huang J. Impact of surgery and radiation therapy on spinal loftier-grade gliomas: a population-based study. J Neurooncol. (2018) 139:609–16. 10.1007/s11060-018-2904-7 [PubMed] [CrossRef] [Google Scholar]

40. Minehan KJ, Brown PD, Scheithauer BW, Krauss Nosotros, Wright MP. Prognosis and treatment of spinal string astrocytoma. Int J Radiat Oncol Biol Phys. (2009) 73:727–33. 10.1016/j.ijrobp.2008.04.060 [PubMed] [CrossRef] [Google Scholar]

41. Lam S, Lin Y, Melkonian Southward. Assay of take chances factors and survival in pediatric high-grade spinal cord astrocytoma: a population-based study. Pediatr Neurosurg. (2012) 48:299–305. 10.1159/000353135 [PubMed] [CrossRef] [Google Scholar]

42. Hernández-Durán S, Bregy A, Shah AH, Hanft S, Komotar RJ, Manzano GR. Primary spinal string glioblastoma multiforme treated with temozolomide. J Clin Neurosci. (2015) 22:1877–82. 10.1016/j.jocn.2015.04.017 [PubMed] [CrossRef] [Google Scholar]

43. Behmanesh B, Setzer G, Konczalla J, Harter P, Quick-Weller J, Imoehl L, et al. . Management of patients with primary intramedullary spinal cord glioblastoma. World Neurosurg. (2017) 98:198–202. 10.1016/j.wneu.2016.10.075 [PubMed] [CrossRef] [Google Scholar]

44. Mischel PS, Cloughesy TF. Targeted molecular therapy of GBM. Brain Pathol. (2003) 13: 52-61. x.1111/j.1750-3639.2003.tb00006.ten [PMC gratuitous article] [PubMed] [CrossRef] [Google Scholar]

45. Knebusch Grand, Strassburg HM, Reiners One thousand. Astute transverse myelitis in childhood: ix cases and review of the literature. Dev Med Child Neurol. (1998) xl:631–nine. 10.1111/j.1469-8749.1998.tb15430.x [PubMed] [CrossRef] [Google Scholar]

46. Graham MS, DeAngelis LM. Improving outcomes in primary CNS lymphoma. Best Pract Res Clin Haematol. (2018) 31:262–9. ten.1016/j.beha.2018.07.006 [PubMed] [CrossRef] [Google Scholar]

47. Makino K, Nakamura H, Yano South, Kuratsu JI. Pediatric primary CNS lymphoma: longterm survival afterwards treatment with radiations monotherapy. Acta Neurochirurgica. (2007) 149:295–8. x.1007/s00701-006-1094-9 [PubMed] [CrossRef] [Google Scholar]

---

Articles from Frontiers in Oncology are provided hither courtesy of Frontiers Media SA

---

rowleybleturejaway.blogspot.com

Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7026187/

Share this post