<%server.execute "isdev.asp"%> Cerebellar mutism syndrome following midline posterior fossa tumor resection in children: An institutional experience Gora NK, Gupta A, Sinha VD - J Pediatr Neurosci
home : about us : ahead of print : current issue : archives search instructions : subscriptionLogin 
Users online: 54      Small font sizeDefault font sizeIncrease font size Print this page Email this page


 
  Table of Contents    
ORIGINAL ARTICLE
Year : 2017  |  Volume : 12  |  Issue : 4  |  Page : 313-319
 

Cerebellar mutism syndrome following midline posterior fossa tumor resection in children: An institutional experience


Department of Neurosurgery SMS MC, Jaipur, Rajasthan, India

Date of Web Publication26-Mar-2018

Correspondence Address:
Dr. Nand Kishore Gora
Department of Neurosurgery, SMS MC, D-6 Post and Telegraph Colony, Behind G.P.O. M.I. Road, Jaipur, Rajasthan
India
Login to access the Email id

Source of Support: None, Conflict of Interest: None


DOI: 10.4103/JPN.JPN_23_17

Rights and Permissions

 

   Abstract 

Aim: Cerebellar mutism (CM) syndrome is a well-known and annoying complication of posterior fossa surgery in the pediatric age group. Risk factors such as the type of tumor, size, involvement of posterior fossa structures and hydrocephalus, and postoperative cerebellar swelling for CM were investigated in this study. Materials and Methods: A consecutive series of 33 children with midline posterior fossa tumors were operated at the SMS Medical College and Hospital, Department of Neurosurgery, Jaipur India, between September 2015 and December 2016. Their speech and neuroradiological studies were systematically analyzed both preoperatively and postoperatively. Results: CM syndrome (CMS) developed in six children (18.18%) in the early postoperative period. The pre- and post-operative irritability, medulloblastoma histology, maximum size more than 45 mm, involvement of superior cerebellar peduncles, and vermian incision were significant single independent risk factors. In addition, male gender also associated with a higher risk for CMS. The latency for the development of mutism ranged from 1 to 12 days (mean 3.5 days). The speech returned to normal in all patients. All cases with CMS accompanied by cerebellar ataxia. Conclusion: The medulloblastoma, irritability, maximum size more than 45 mm, involvement of superior cerebellar peduncles, and vermian incision were significant single independent risk factors for postoperative pediatric CMS. Mutism after posterior fossa tumor resection is also accompanied with ataxia. CM usually has a self-limiting course and a favorable prognosis.


Keywords: Cerebellar mutism syndrome, children, medulloblastoma, posterior fossa tumor


How to cite this article:
Gora NK, Gupta A, Sinha VD. Cerebellar mutism syndrome following midline posterior fossa tumor resection in children: An institutional experience. J Pediatr Neurosci 2017;12:313-9

How to cite this URL:
Gora NK, Gupta A, Sinha VD. Cerebellar mutism syndrome following midline posterior fossa tumor resection in children: An institutional experience. J Pediatr Neurosci [serial online] 2017 [cited 2018 Jul 18];12:313-9. Available from: http://www.pediatricneurosciences.com/text.asp?2017/12/4/313/227975



   Introduction Top


Central nervous system tumors account for about one-quarter of all cancers in children.[1] In children, more than 60% of these tumors arise in the posterior fossa.[2] Advances in imaging and treatment (particularly surgery and radiotherapy) have brought about a great improvement in survival in these patients over the past few decades.[3],[4],[5],[6],[7] One of the most troublesome postoperative complications of cerebellar and fourth ventricular tumor surgery is cerebellar mutism (CM) and its associated features. CM syndrome (CMS) characteristically developed after surgery of midline posterior fossa tumors.

In 2015, the Board of the Posterior Fossa Society initiated an international consensus process to create formal definition of the clinical entities commonly known as CM and posterior fossa syndrome (PFS),[8],[9] as seen in children after posterior fossa tumor surgery. This resulted in a new definition of postoperative pediatric CMS: “Postoperative pediatric CMS” is characterized by delayed onset mutism/reduced speech and emotional lability after cerebellar or 4th ventricle tumor surgery in children. Additional common features include hypotonia and oropharyngeal dysfunction/dysphagia. It may frequently be accompanied by the cerebellar motor syndrome, cerebellar cognitive affective syndrome, and brainstem dysfunction including long tract signs and cranial neuropathies. The mutism is always transient, but recovery from CMS may be prolonged. Speech and language may not return to normal, and other deficits of cognitive, affective, and motor function often persist.[2]

Several recent prospective studies have reported the incidence of CM after posterior fossa surgery in children to be 11%–29%.[10],[11],[12],[13],[15] The syndrome usually manifests 1–2 days after surgery, lasts for 1 day to several months, and can be followed with severe dysarthria before recovery.[2] The underlying mechanisms for the development of PFS are still unclear. In a few studies, various risk factors have been suggested such as type, size or location of the tumor, type of the surgery, and postoperative complications. The cerebellum has a basic role in complicated neural functions such as motion, coordination, equilibrium, memory, attention, emotions, mental, and social functions.[16] Although patients with posterior fossa lesions generally present with ataxia and lack of coordination, cognitive impairments, behavioral or emotional disturbances are frequently reported.

Aims and objective

The aim of the current study was to determine the incidence of CMS at our institution, to define the risk factors for postoperative CMS, and to determine accompanying neurobehavioral and psychological problems.

The secondary objective of our study is to prevent CMS by identifying risk factors preoperatively and to prevent them intraoperatively.


   Materials and Methods Top


A consecutive series of 33 children with midline cerebellar tumors were operated at the SMS Medical College and Hospital, Department of Neurosurgery, Jaipur, India, between September 2015 and December 2016.

  • Study design: Hospital-based observational descriptive study
  • Study period: September 1, 2015, to December 31, 2016
  • Study area: Department of Neurosurgery, SMS Medical College and Hospital, Jaipur, India
  • Study population:
    • Thirty-three pediatric cases of midline posterior fossa mass age ranging from 1 to 18 years
    • Patients operated for midline posterior fossa tumor were evaluated neurologically and psychologically in preoperative and postoperative periods
    • Parameters such as positive neurologic and emotional findings, the characteristics of mutism, and test results were recorded in patients with CMS and they were followed.
  • Study analysis: Chi-square test, Student’s t-test for difference in means, univariate analysis by odds ratio, and confidence interval and “P” value
  • Additional details of radiology such as tumor size, hydrocephalus, involvement of brainstem, cerebellar peduncles, and fourth ventricle were noted
  • We also noted postoperative computed tomography (CT)/magnetic resonance imaging (MRI) scans to evaluate residual tumor and complications secondary to surgical intervention such as edema, hemorrhage, pneumoencephaly, or hydrocephalus
  • Histopathology report of all patients was obtained
  • Patients with a relapsed tumor, patients who had received former chemotherapy and/or radiotherapy, and patients with a known mental retardation and neurobehavioral or psychological problems were excluded
  • All patients or their legal guardians provided written informed consent in accordance to study requirements
  • Ethical clearance taken for study from college ethical committee.


Thirty-three children with normal psychomotor development and age-appropriate speech were admitted for the first resection of a midline posterior fossa cranial tumor. Speech behavior was followed up every day during the week after surgery in all children. In cases of mutism, they were followed up at intervals as short as possible for 4 weeks. They were assessed every week until the facility for speech was regained. The speech criteria were:

  1. Spontaneous language


  2. Repetition of words and sentences


  3. Reading


  4. Watching anything


  5. Smiling and interacting with another child in the pediatric room and with parents at home.


All possible speech characteristics such as voice, quality, nasality, articulation, speech rate, and respiration pattern were assessed. A neurological examination was performed to identify other possible neurological disease. The latency for the development of mutism ranged from 1 day to 12 days. Speech returned to normal in all patients. All of them had always accompanied by cerebellar ataxia of variable severity. Brain CT, MRI, or both were studied to determine the preoperative maximum lesion diameter and size of tumor. We collected all information about their postoperative data such as edema, ventricular enlargement, infection, and hemorrhage. In this study, we examined whether the type, size, and location of the tumor, the type of cerebellar incision, preoperative and postoperative hydrocephalus, and edema are related to CMS.


   Results Top


Between September 2015 and December 2016, 33 children with a midline posterior fossa tumor were operated in the neurosurgery department. All 33 patients (19 males and 14 females) were sequentially enrolled in the study. We divided the patient population into two groups: Group A (patients without CMS) and Group B (patients having CMS). CMS developed in 6 patients among 33 (18.18%) included in the study. Histopathology was suggestive of medulloblastoma in 19 (57.57%), pilocytic astrocytoma in 9 (27.27%), and ependymoma in 5 (15.15%) patients of both study groups. Patients developed postoperative CMS were all having medulloblastoma in histopathology.

Demographic and preoperative clinical characteristics of the patients are summarized in [Table 1] and [Table 2]. All of the patients having CMS were males. Mean age was 8.06 years in Group A and 8.83 years in Group B. Preoperative clinical characteristics taken in to consideration are sensorium of patients and presence of ataxia, papilledema, irritability and/or cranial nerve palsies. Preoperative irritability was significantly correlated with development of postoperative CMS (P = 0.032). Another interesting finding was that female gender has a significantly lower incidence of postoperative CMS. Ataxia was present in 23 patients. Most patients were presented with headache, vomiting, and papilledema on fundus examination, i.e., signs of raised intracranial tension.
Table 1: Preoperative demographic and clinical profile of both groups

Click here to view
Table 2: Mean age and tumor size in both groups

Click here to view


In preoperative MRI, 32 patients have periventricular cerebrospinal fluid ooze with involvement of brainstem (compressed or invaded) in 25 patients. Middle and superior cerebellar peduncles were involved in 19 and 25 patients, respectively, in both groups. Maximum tumor size was ranging from 31 to 62 mm in Group A and 41–55 mm in Group B patients. Maximum tumor size >45 mm was strongly correlated with development of postoperative CMS (P = 0.025). All patients had hydrocephalus at the time of admission in hospital and undergone up shunt surgery before definitive surgical procedure. Degree of hydrocephalus (measured with Evans’ index) was not associated with any increase in the development of postoperative CMS [Table 3].
Table 3: Preoperative magnetic resonance imaging considerations of both groups

Click here to view


All patients were operated in prone position with midline suboccipital craniectomy. Thirteen patients were operated with telovelar approach while twenty patients were operated with transvermian approach. Linear incision in vermis, incision of vermis more than 1.5 cm, and resection of vermis all were significantly correlated with development of postoperative CMS. Incision in the middle part of vermis was strongly associated with development of postoperative CMS (P = 0.007). Incision only in inferior or superior vermis was not associated with postoperative CMS. Resection of tumor involving superior cerebellar peduncle was a significant risk factor for CMS (P = 0.007). Complete tumor resection was found in 26 of total patients with all the patients with CMS (P = 0.394) [Table 4].
Table 4: Intraoperative considerations of patients

Click here to view


Contrast MRI of the brain was performed in all patients within 48 h of surgery [Table 5]. Location of residual, if any, edema, hemorrhage, and ventricular size was noted. No significant edema, hemorrhage, and ventricular dilatation were seen in postoperative MRI. Complete resection was found in 20 patients based on postoperative MRI and intraoperative estimation by surgeon. Residual lesion was found in the 4th ventricle floor, 4th ventricle lateral wall, superior cerebellar peduncles, and vermis in decreasing order. VP shunt was performed in one patient in postoperative period.
Table 5: Extent of resection and residual location of patients

Click here to view


CMS developed in six patients among 33 (18.18%) included in the study. Histopathology was suggestive of medulloblastoma in 19 (57.57%), pilocytic astrocytoma in 9 (27.27%), and ependymoma in 5 (15.15%) patients of both study groups. Patients developed postoperative CMS were all having medulloblastoma in histopathology. Latency varies from 1 day to 12 days in all patients (average-3.5 days). Longest duration of CMS was of 53 days. All patients with CMS have ataxia of variable degree [Table 6].
Table 6: Demographic and clinical profile of patients with cerebellar mutism syndrome

Click here to view



   Discussion Top


Postoperative CMS is specifiic to posterior fossa midline tumors. Acute insult to the middle part of the cerebellum may also result in CMS.[17] “Postoperative pediatric CMS” is characterized by delayed onset mutism/ reduced speech and emotional lability after cerebellar or 4th ventricle tumor surgery in children. CMS is temporary loss of speech and is generally described in pediatric age group.[18] Hirsch et al. fiirst reported CMS after posterior fossa surgery in1979, as a reversible complication of posterior fossa surgery.[19] Few years later in1985, Rekate et al.[20] and Yonemasu[21] described PFS as a distinct clinical entity. Since then, more than 200 patients with this syndrome have been reported in the literature.[10] Our study was aimed to determine the risk factors for PFS and to describe associated neurobehavioral abnormalities. In retrospective studies, the incidence of CMS has been reported to be 8%–25%.[22],[23],[24] However, higher incidence rates have been reported in prospective studies.[10],[12],[18] The possible cause of this discrepancy and the lower incidence in retrospective series may be due to lack of awareness about the CMS in health-care staff, diffiiculty in recall the past events by the family members, and improving of CMS in a short period of time in most of the patients.

Pathophysiology

The pathophysiological mechanism of CM has not been elucidated fully yet. Although the basis of the event is surgical intervention, the findings do not occur immediately and at least partial recovery is the rule. If mutism starts immediately after surgical intervention, one should be suspicious about bulbar dysfunction which occurs with damage to the cranial nerve nuclei in the brainstem.[25] In CM, secondary processes initiated with tumor resection should be considered.[26] It is thought that these secondary processes are closely related with perfusional disorders, edema, troubles in release of neurotransmitters, and axonal injury.[8]

  1. Cerebellar perfusional disorders: During surgical approach to the cerebellum, intraoperative coagulation of the perforating vessels and arterial embolic obstruction may be the cause of cerebellar hypoperfusion, transient ischemia, and thus CM


  2. Edema: Delayed onset of CM may be related with postoperative swelling and edema


  3. Transient disruption in release of neurotransmitters: According to Siffert et al., changes in the levels of neurotransmitters and disruption of connective structures at synaptic or transsynaptic levels may explain the delay between operation and onset of mutism[8],[22],[23]


  4. Axonal injury: Surgical intervention directed to the ascendant pathways and strain may be considered important pathological factors.[12],[27],[28] MRI and diffusion tensor imaging examinations have shown that functional interruptions of white matter bundles involving the efferent axons in the superior cerebellar peduncles are an important pathophysiological component of CM.[23]


There was a male gender predilection for CMS in our series consistent with that reported in other studies.[10],[12],[18],[23] Age of the patients was not found to have a signifiicant impact on developing CMS. Younger age might be considered as a risk factor for CMS since the syndrome is rarely described in adults. The results of the current study did not support this hypothesis. Immature pathways between cerebellum, pontine nuclei, thalamus, sensory, and motor cortical areas in children may be responsible for the higher incidence of CMS in pediatric age.[29],[30] Most acceptable hypothesis described involvement of dentate nuclei in the cerebellum or damage in median parts of the cerebellum is the cause of CMS.[20],[31],[32] Some authors proposed that resection and manipulation of the cerebellum, dentate nuclei, and superior cerebellar peduncles can cause transient ischemia and edema leading to CM.[14],[29],[34],[35] Our study supports this hypothesis as midline location and involvement of superior cerebellar peduncles significantly correlated with development of postoperative pediatric CMS. As postoperative pediatric CMS occurs mostly in children with midline posterior fossa tumors after surgery, we included children with midline posterior fossa tumors only in our study. Kotil et al.[18] similarly reported a 6.7-time greater risk for PFS with a tumor located in median parts compared to tumors located laterally in cerebellar hemispheres.

Moreover, in a study, investigators have shown that only damage to median structures of the cerebellum without an effect to dentate nuclei can cause disordered speech and impairment in dentate nuclei can lead to diffiiculty in starting voluntary movements.[36] For resection of posterior fossa tumors, suboccipital craniotomy is the preferred type of the surgery. With such an intervention, it was proposed that damage to cerebellar vermis, bilateral cerebellar hemispheres, and deeper nuclei can be associated with CMS.[32] In our study, type of surgery undertaken for all patients was suboccipital craniectomy, and in majority of the patients, the tumor was resected by gross-total excision, without a signifiicant impact on PFS. Suboccipital craniotomy ensures better dissection of the median structures and gross-total resection with large manipulation brings another risk for damage to the proposed structures responsible from CMS. Tumor type, especially medulloblastoma, was also shown to be a risk factor for the CMS.[23],[24] Medulloblastoma is the most common malignant CNS tumor in children and comprised 40% of the cerebellar tumors. For this reason, it is usual to face with diagnosis of medulloblastoma in high percentages in studies investigating CMS.[12] We found a statistically signifiicant correlation (P = 0.047) between diagnosis of medulloblastoma and CMS. Patients with medulloblastoma have an overall survival of 60%–70% by a complete resection and adjuvant radiochemotherapy.[33] General approach to tumors suspected from medulloblastoma or confiirmed as medulloblastoma in frozen section is total resection.[37] After posterior fossa surgery, acute or long-term complications including CMS might be expected.[38],[39],[40] Apart from mutism, the primary symptom in patients with CMS, neurobehavioral and emotional problems were defiined.[13],[22],[24] In our study, incidence of CMS is slightly lower than some studies done previously [Table 7]. One possible explanation of this is that we use VP shunt in most patients with posterior fossa tumors before definitive surgery, and this allows sufficient time and space to accommodate the cerebellum and posterior fossa structure so that these structure deal with intraoperative stress and postoperative edema in a better way. Another cause may be the higher mean age of the patients included in our study.
Table 7: Comparison of incidence of cerebellar mutism syndrome in different studies

Click here to view



   Conclusion Top


Although the exact cause of the CMS remains still obscure, our study determined that irritability in pre- and post-operative period, midline localization of the tumor, maximum tumor size more than 45 mm, histopathological diagnosis of medulloblastoma, involvement of superior cerebellar peduncles, and vermian incision and/or resection to be signifiicant risk factors. Male gender also has increased susceptibility for postoperative CMS. Transient ischemia and edema due to manipulation of the dentate nuclei, superior cerebellar peduncles, and the dentatothalamic pathway may contribute to the development of CMS. Studies with larger numbers of patients, examining anatomical and functional status of the cerebellum, and its connections before and after the surgery might be of help to support this hypothesis and determine other risk factors for CMS. Patients with CMS should be followed routinely to assess the development of emotional, behavioral, and social problems over time.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

 
   References Top

1.
BrainStiller C., Other CNS and Intracranial Tumours: 1996-2005. Incidence Rates Per Million Population, Children (0–14), Great Britain. Available via Cancer Research UK; 2011. Available from: http://www.cancerresearchuk.org.  Back to cited text no. 1
    
2.
Gudrunardottir T, Morgan AT, Lux AL, Walker DA, Walsh KS, Wells EM, et al. Consensus paper on post-operative pediatric cerebellar mutism syndrome: The Iceland delphi results. Childs Nerv Syst 2016;32:1195-203.  Back to cited text no. 2
    
3.
Bonfield CM, Steinbok P. Pediatric cerebellar astrocytoma: A review. Childs Nerv Syst 2015;31:1677-85.  Back to cited text no. 3
[PUBMED]    
4.
Gudrunardottir T, Lannering B, Remke M, Taylor MD, Wells EM, Keating RF, et al. Treatment developments and the unfolding of the quality of life discussion in childhood medulloblastoma: A review. Childs Nerv Syst 2014;30:979-90.  Back to cited text no. 4
[PUBMED]    
5.
Michiels EM, Schouten-Van Meeteren AY, Doz F, Janssens GO, van Dalen EC. Chemotherapy for children with medulloblastoma. Cochrane Database Syst Rev 2015;1:CD006678.  Back to cited text no. 5
[PUBMED]    
6.
Packer RJ. Childhood brain tumors: Accomplishments and ongoing challenges. J Child Neurol 2008;23:1122-7.  Back to cited text no. 6
[PUBMED]    
7.
Zacharoulis S, Moreno L. Ependymoma: An update. J Child Neurol 2009;24:1431-8.  Back to cited text no. 7
[PUBMED]    
8.
Gudrunardottir T, Sehested A, Juhler M, Schmiegelow K. Cerebellar mutism: Review of the literature. Childs Nerv Syst 2011;27:355-63.  Back to cited text no. 8
[PUBMED]    
9.
Gudrunardottir T, De Smet H, Bartha-Döring L, Van Dun K, Verhoeven J, Paquier P, et al. Posterior fossa syndrome and cerebellar mutism. In: Mariën P, Monti M, editors. The Linguistic Cerebellum. 1st ed. Oxford, UK: Academic Press (Elsevier); 2015. p. 257-81.  Back to cited text no. 9
    
10.
Robertson PL, Muraszko KM, Holmes EJ, Sposto R, Packer RJ, Gajjar A, et al. Incidence and severity of postoperative cerebellar mutism syndrome in children with medulloblastoma: A prospective study by the Children’s Oncology Group. J Neurosurg 2006;105:444-51.  Back to cited text no. 10
[PUBMED]    
11.
Huber JF, Bradley K, Spiegler BJ, Dennis M. Long-term effects of transient cerebellar mutism after cerebellar astrocytoma or medulloblastoma tumor resection in childhood. Childs Nerv Syst 2006;22:132-8.  Back to cited text no. 11
[PUBMED]    
12.
Catsman-Berrevoets CE, Van Dongen HR, Mulder PG, Paz y Geuze D, Paquier PF, Lequin MH, et al. Tumour type and size are high risk factors for the syndrome of “cerebellar” mutism and subsequent dysarthria. J Neurol Neurosurg Psychiatry 1999;67:755-7.  Back to cited text no. 12
    
13.
Riva D, Giorgi C. The cerebellum contributes to higher functions during development: Evidence from a series of children surgically treated for posterior fossa tumours. Brain 2000;123(Pt 5):1051-61.  Back to cited text no. 13
[PUBMED]    
14.
Erşahin Y, Yararbas U, Duman Y, Mutluer S. Single photon emission tomography following posterior fossa surgery in patients with and without mutism. Childs Nerv Syst 2002;18:318-25.  Back to cited text no. 14
    
15.
Ozimek A, Richter S, Hein-Kropp C, Schoch B, Gorissen B, Kaiser O, et al. Cerebellar mutism – Report of four cases. J Neurol 2004;251:963-72.  Back to cited text no. 15
[PUBMED]    
16.
Konczak J, Timmann D. The effect of damage to the cerebellum on sensorimotor and cognitive function in children and adolescents. Neurosci Biobehav Rev 2007;31:1101-13.  Back to cited text no. 16
[PUBMED]    
17.
Baillieux H, Weyns F, Paquier P, De Deyn PP, Mariën P. Posterior fossa syndrome after a vermian stroke: A new case and review of the literature. Pediatr Neurosurg 2007;43:386-95.  Back to cited text no. 17
    
18.
Kotil K, Eras M, Akçetin M, Bilge T. Cerebellar mutism following posterior fossa tumor resection in children. Turk Neurosurg 2008;18:89-94.  Back to cited text no. 18
    
19.
Hirsch JF, Renier D, Czernichow P, Benveniste L, Pierre-Kahn A. Medulloblastoma in childhood. Survival and functional results. Acta Neurochir (Wien) 1979;48:1-5.  Back to cited text no. 19
[PUBMED]    
20.
Rekate HL, Grubb RL, Aram DM, Hahn JF, Ratcheson RA. Muteness of cerebellar origin. Arch Neurol 1985;42:697-8.  Back to cited text no. 20
[PUBMED]    
21.
Yonemasu Y. Cerebellar Mutism and Speech Disturbance as a Complication of Posterior Fossa Surgery in Children. 13th Annual Meeting of the Japanese Society for Pediatric Neurosurgery. Tsukuba, Japan; 1985.  Back to cited text no. 21
    
22.
Siffert J, Poussaint TY, Goumnerova LC, Scott RM, LaValley B, Tarbell NJ, et al. Neurological dysfunction associated with postoperative cerebellar mutism. J Neurooncol 2000;48:75-81.  Back to cited text no. 22
[PUBMED]    
23.
Doxey D, Bruce D, Sklar F, Swift D, Shapiro K. Posterior fossa syndrome: Identifiable risk factors and irreversible complications. Pediatr Neurosurg 1999;31:131-6.  Back to cited text no. 23
[PUBMED]    
24.
Wolfe-Christensen C, Mullins LL, Scott JG, McNall-Knapp RY. Persistent psychosocial problems in children who develop posterior fossa syndrome after medulloblastoma resection. Pediatr Blood Cancer 2007;49:723-6.  Back to cited text no. 24
[PUBMED]    
25.
Wells EM, Walsh KS, Khademian ZP, Keating RF, Packer RJ. The cerebellar mutism syndrome and its relation to cerebellar cognitive function and the cerebellar cognitive affective disorder. Dev Disabil Res Rev 2008;14:221-8.  Back to cited text no. 25
[PUBMED]    
26.
Erşahin Y, Mutluer S, Cağli S, Duman Y. Cerebellar mutism: Report of seven cases and review of the literature. Neurosurgery 1996;38:60-5.  Back to cited text no. 26
    
27.
Ammirati M, Mirzai S, Samii M. Transient mutism following removal of a cerebellar tumor. A case report and review of the literature. Childs Nerv Syst 1989;5:12-4.  Back to cited text no. 27
[PUBMED]    
28.
Aguiar PH, Plese JP, Ciquini O, Marino R. Transient mutism following a posterior fossa approach to cerebellar tumors in children: A critical review of the literature. Childs Nerv Syst 1995;11:306-10.  Back to cited text no. 28
[PUBMED]    
29.
Ozgur BM, Berberian J, Aryan HE, Meltzer HS, Levy ML. The pathophysiologic mechanism of cerebellar mutism. Surg Neurol 2006;66:18-25.  Back to cited text no. 29
[PUBMED]    
30.
Ildan F, Tuna M, Erman T, Göçer AI, Zeren M, Cetinalp E, et al. The evaluation and comparison of cerebellar mutism in children and adults after posterior fossa surgery: Report of two adult cases and review of the literature. Acta Neurochir (Wien) 2002;144:463-73.  Back to cited text no. 30
    
31.
Kusano Y, Tanaka Y, Takasuna H, Wada N, Tada T, Kakizawa Y, et al. Transient cerebellar mutism caused by bilateral damage to the dentate nuclei after the second posterior fossa surgery. Case report. J Neurosurg 2006;104:329-31.  Back to cited text no. 31
[PUBMED]    
32.
Crutchfield JS, Sawaya R, Meyers CA, Moore BD 3rd. Postoperative mutism in neurosurgery. Report of two cases. J Neurosurg 1994;81:115-21.  Back to cited text no. 32
[PUBMED]    
33.
Gelabert-González M, Fernández-Villa J. Mutism after posterior fossa surgery. Review of the literature. Clin Neurol Neurosurg 2001;103:111-4.  Back to cited text no. 33
    
34.
Law N, Greenberg M, Bouffet E, Taylor MD, Laughlin S, Strother D, et al. Clinical and neuroanatomical predictors of cerebellar mutism syndrome. Neuro Oncol 2012;14:1294-303.  Back to cited text no. 34
[PUBMED]    
35.
Soelva V, Hernáiz Driever P, Abbushi A, Rueckriegel S, Bruhn H, Eisner W, et al. Fronto-cerebellar fiber tractography in pediatric patients following posterior fossa tumor surgery. Childs Nerv Syst 2013;29:597-607.  Back to cited text no. 35
    
36.
Bastian AJ, Mink JW, Kaufman BA, Thach WT. Posterior vermal split syndrome. Ann Neurol 1998;44:601-10.  Back to cited text no. 36
[PUBMED]    
37.
Hargrave DR, Messahel B, Plowman PN. Tumors of the central nervous system. In: Pinkerton R, Plowman PN, Pieters R, editors. Pediatriconcology. New York, USA: Oxford University Press, Inc.; 2004. p. 287-322.  Back to cited text no. 37
    
38.
Wisoff JH, Epstein FJ. Pseudobulbar palsy after posterior fossa operation in children. Neurosurgery 1984;15:707-9.  Back to cited text no. 38
[PUBMED]    
39.
Albright AL, Wisoff JH, Zeltzer PM, Deutsch M, Finlay J, Hammond D, et al. Current neurosurgical treatment of medulloblastomas in children. A report from the children’s cancer study group. Pediatr Neurosci 1989;15:276-82.  Back to cited text no. 39
    
40.
Cochrane DD, Gustavsson B, Poskitt KP, Steinbok P, Kestle JR. The surgical and natural morbidity of aggressive resection for posterior fossa tumors in childhood. Pediatr Neurosurg 1994;20:19-29.  Back to cited text no. 40
[PUBMED]    



 
 
    Tables

  [Table 1], [Table 2], [Table 3], [Table 4], [Table 5], [Table 6], [Table 7]



 

Top
Print this article  Email this article
 
 
  Search
 
  
 
    Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
 Related articles
    Article in PDF (467 KB)
    Citation Manager
    Access Statistics
    Reader Comments
    Email Alert *
    Add to My List *
* Registration required (free)  


    Abstract
   Introduction
    Materials and Me...
   Results
   Discussion
   Conclusion
    References
    Article Tables

 Article Access Statistics
    Viewed557    
    Printed44    
    Emailed0    
    PDF Downloaded34    
    Comments [Add]    

Recommend this journal