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DOI: 10.1055/s-0044-1801404
Cerebellar Mutism/Posterior Fossa Syndrome Following Resection of Posterior Fossa Tumor in Pediatric Patients: Assessing Pathophysiology, Risk Factors, and Neuroradiographic Features
- Abstract
- Introduction
- Materials and Methods
- Statistical Analysis
- Results
- Discussion
- Conclusion
- References
Abstract
Background
Cerebellar mutism syndrome (CMS) is a postoperative syndrome of decreased speech seen in children associated with neurobehavioral abnormalities, the incidence of which is up to 40%.
Objectives
To evaluate pediatric patients with posterior fossa tumors for incidence, clinical characteristics, pathophysiology, risk factors, and neuroradiographic features of this syndrome.
Materials and Methods
The study included 60 pediatric patients with a posterior fossa tumor who underwent surgery by a telovelar approach. Detailed pre- and postoperative clinical and radiological evaluations were done. Patients with CMS were analyzed and compared with those without mutism to find risk factors for CMS. The presentation and characteristics of cerebellar mutism were studied along with the following risk factors:
-
Clinical—age, sex, cranial nerve deficit, and adjuvant treatment.
-
Radiological—tumor location, hydrocephalus, brainstem invasion, extent of tumor resection, peduncular and brainstem edema, and atrophy of posterior fossa structures.
-
Pathological—histopathology of tumor.
The preoperative, immediate postoperative, and 1-year postoperative imaging results were reviewed to assess the neuroradiographic features in the two groups.
Results
The incidence of this syndrome was 20%. The mutism was accompanied by some neurobehavioral abnormalities (p-value = 0.05). The most significant finding was the presence of a period of cerebellar dysarthria after the resolution of the muteness (p-value < 0.001) in all cases. Brainstem and related structures' involvement was the most significant risk factor (p-value = 0.03). The presence of brainstem and peduncular edema in the immediate postoperative period (p-value = 0.04) and gross atrophy of posterior fossa structures at 1 year (p-value = 0.01) showed significance toward the development of CMS. There was delayed neurological recovery in patients with CMS with a poor Glasgow Outcome Score at 1 year of follow-up.
Conclusion
The clinical presentation of this syndrome in context with neuroradiographic features suggests that it results from transient impairment of the afferent and/or efferent pathways of dentate nuclei that are involved in initiating complex volitional movements and are associated with brainstem involvement of tumor and poor functional outcome.
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Keywords
mutism - neurobehavioral - dysarthria - posterior fossa tumors in children - posterior fossa syndromeIntroduction
Cerebellar mutism (CM) is a term used to describe the lack of speech caused by lesions of the cerebellum, which is not associated with long tract signs, or alteration of consciousness and usually appears because of posterior fossa surgery in children with posterior fossa tumors[1] and rarely infections,[2] posterior fossa hematomas, arteriovenous malformations, brainstem tumor, pineal gland tumor, and traumatic cerebellar injury. There are rare reports of CM in adults and the higher incidence in the pediatric population may be related to the higher incidence of posterior fossa tumors in children.[3]
A synonym for CM is transient CM, emphasizing the short duration. The term cerebellar mutism syndrome (CMS) is used to describe a group of symptoms caused by a cerebellar lesion, including muteness, ataxia, hypotonia, and irritability, while mutism and subsequent dysarthria[4] are used to describe the linguistic part of CM. Posterior fossa syndrome (PFS) is a broader term that includes CM and, in addition, movement disorders (ataxia and hypotonia) and a wide spectrum of neurobehavioral abnormalities.[5] CMS is regarded as a synonym for PFS and these terms can be used interchangeably.[1]
The incidence of PFS may reach as high as 40%.[6] Even after substantial improvements in neurosurgical techniques and consequently reduction in overall surgical morbidity and mortality, the incidence of PFS continues to increase in the modern neurosurgical era. This may be due to wider recognition of this neurological and neurobehavioral syndrome. However, posterior fossa tumor removal remains challenging and far from risk-free especially in developing children. The predictive factors that place patients at risk for developing PFS and how to prevent this phenomenon remain to be elucidated.
The aim of this study was to evaluate the incidence and the clinical characteristics of CMS in pediatric patients with posterior fossa tumors and to elucidate the pathophysiological basis and predictive risk factors for this syndrome and assess the associated neuroradiographic features.
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Materials and Methods
The study was a prospective study, conducted at a tertiary care neurosurgery center, GIPMER (G.B. Pant Institute of Post Graduate Medical Education and Research), New Delhi for a period of 18 months from January 2023 to August 2024. The cohort was recruited in the first 6 months of the indicated period and followed up for 1 year. ([Fig. 1])


Inclusion criteria were pediatric patients of all age groups (1 month–18 years) who were diagnosed to have posterior cranial fossa tumors on imaging whether primary or metastasis, benign or malignant.
The exclusion criteria were patients more than 18 years of age, tumors of supratentorial or spinal origin with an extension into the posterior fossa, and recurrent posterior fossa tumors. The recorded data included age and sex distribution, duration and nature of symptoms, detailed clinical evaluation, radiological analysis, intraoperative assessment of tumor, histological examination, and postoperative neurological examination.
Mutism was defined as the total absence of speech and sound in an awake and conscious patient, not associated with long tract signs, or alteration of consciousness, and following posterior fossa surgery in children. Since mutism usually does not occur as an isolated entity, the presence of any associated motor disorder like ataxia, axial hypotonia, and neurobehavioral disturbance was also assessed, which included curling up in bed, emotional lability, oropharyngeal apraxia, uncontrollable crying, apathy, irritability, loss of bladder, and bowel control.
The tumor was classified into four regions based on the likely site of origin and epicenter of the tumor: (1) vermian, (2) vermian with lateral extension, (3) hemispheric, and (4) predominantly affecting brainstem.
Preoperative imaging, including computed tomography (CT) and magnetic resonance imaging (MRI) studies, was reviewed for each affected patient in parallel with age-matched patients with posterior fossa tumors who did not develop mutism. In all patients, postoperative images were obtained within 48 hours of operation and at 1 year. The images were graded based on the location of the lesion; tumor involvement of the cerebellum, cerebellar peduncles, and brainstem; preoperative edema, and postoperative edema or hemorrhage. The patients were analyzed for development and persistence of symptoms within 48 hours postoperatively, at 3 months, and 1 year respectively to assess for evidence of permanent injury. The neurological outcome was assessed at 1-year follow-up based on the Glasgow Outcome Scale (GOS).
The presentation and characteristics of CM were studied along with the following risk factors:
-
Clinical—age, sex, cranial nerve deficit, and adjuvant treatment.
-
Radiological—tumor location, hydrocephalus, brainstem invasion, extent of tumor resection, peduncular and brainstem edema, and atrophy of posterior fossa structures.
-
Pathological—histopathology of tumor.
The surgical approach and technique used in the two groups were essentially similar and involved a telovelar approach with minimal retraction of the vermis and related structures.
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Statistical Analysis
Data were coded and recorded in MS Excel software. Parametric variables were examined for significance using Student's t-test. Nonparametric variables were examined using a Chi-square test. p-Value less than 0.05 was considered significant.
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Results
A total of 60 cases of posterior fossa space-occupying lesions were included in the study. There was a preponderance of the male population comprising 36 patients (60%). The age of the pediatric population ranged from 30 months to 16 years. The average age was 7.65 years.
The most common tumor in the pediatric population was medulloblastoma (n = 24, 40%), followed by pilocytic astrocytoma (n = 12, 20%), ependymoma (n = 12, 20%), glioma (n = 6, 10%), and miscellaneous cases including 4 cases of dermoid and 2 choroid plexus papilloma.
[Table 1] and [Fig. 2] summarize the comparison between patients with and without CM. The mean age, sex distribution, and presence of hydrocephalus did not differ significantly. Eight of the 24 lesions located in the vermis and 4 of the 16 located in the vermis with extension into cerebellar hemispheres showed postoperative mutism. Mutism was not present in either of the 14 patients with a purely hemispheric tumor or the 4 patients with tumors predominantly affecting the brainstem.
Factors |
CMS present |
CMS absent |
p-Value |
---|---|---|---|
No. of patients |
12 (20%) |
48 (80%) |
|
Mean age at diagnosis |
7.1 years |
8.2 years |
0.68 |
Gender |
|||
Male |
8 |
28 |
0.65 |
Female |
4 |
20 |
|
Tumor localization |
0.27 |
||
Vermis |
8 (66.6%) |
16 (33%) |
|
Vermis with lateral extension |
4 (25%) |
12 (25%) |
|
Hemispheric |
0 |
14 |
|
Predominantly brainstem |
0 |
6 |
|
Brainstem and related structures' invasion |
10 (83.3%) |
16 (33.3%) |
0.03[a] |
Preoperative hydrocephalus |
6 (50%) |
32 (66.6%) |
0.45 |
Cranial nerve deficit |
0.56 |
||
Oculomotor |
8 (66.6%) |
20 (41.6%) |
|
Facial |
4 (33.3%) |
6 (12.5%) |
|
Lower cranial nerves |
0 |
4 (8.3%) |
|
Postoperative dysarthria |
12 (100%) |
4 (8.3%) |
<0.001[a] |
Neurobehavioral disturbance |
8 (66.6%) |
6 (12.5%) |
0.005[a] |
Post-op adjuvant treatment: |
10 (83.3%) |
34 (66.6%) |
0.54 |
Abbreviation: CMS, cerebellar mutism syndrome.
a Significant.


Brainstem invasion or involvement was significant (p-value = 0.03; [Fig. 3A]); observed in 10 patients with mutism and in 16 patients without CMS. Cranial nerve deficits (p-value = 0.056) were not significantly more frequent in the patients suffering from CM: oculomotor disturbances were found in 20 of 48 patients without CM versus 8 of 10 in the mute group; facial nerve paresis occurred in 6 of the 48 patients without CM versus 6 of 10 in the mute group; and lower cranial nerve dysfunction occurred only in 4 of the 48 patients without CM and no case of lower cranial nerve deficit was seen in the mute group.


Six children in the study had dysarthria, while 12 had mutism. Postoperative dysarthria was the most significant finding found in all the 12 patients after their recovery from mutism (p-value = 0.001). Neurobehavioral disturbance was a significant finding (p-value = 0.005) and was found in 8 of the 12 children associated with CM (emotional lability and irritability in 6 patients). Neurobehavioral disturbances included oropharyngeal apraxia in 2, inconsolable crying in 2, impairment of volitional activity in 2, and emotional lability and irritability in 6 patients.
The time course of clinical improvement varied significantly among patients. All patients recovered with some degree of vocalization within 3 months of surgery with all the cases presenting with initial dysarthria in the recovery phase. Eight of the children with CMS had residual ataxia interfering with routine functioning at 3 months, although the neurobehavioral abnormality and mutism had completely resolved, however, cranial nerve deficit persisted in eight patients at 1 year. Dysarthria resolved in all patients at 1-year follow-up. Eight patients had ataxia interfering with normal functioning at 1 year.
Neuroradiographic Features in Immediate Postoperative Period
Differences in immediate postoperative imaging between patients with and without PFS are tabulated in [Table 2]. Cerebellar edema was observed in almost 80 to 90% of all patients with and without PFS. Peduncular edema showed (p-value = 0.04) significance in patients with PFS. There was no difference in terms of overall surgical technique and approach in the two groups of patients. In both groups, 90% of patients underwent near-total tumor excision (p-value = 0.54; leaving the tumor tissue attached to major neurovascular structures) via the telovelar approach (associated with limited retraction). No association was seen with the development of postoperative hydrocephalus (p-value = 0.67).
Neuroradiographic features |
CMS present |
CMS absent |
p-Value |
---|---|---|---|
No. of patients |
12 |
48 |
|
Cerebellar edema |
10 (83.3%) |
44 (91.6%) |
0.54 |
Brainstem edema |
6 (50%) |
20 (41.6%) |
0.71 |
Peduncular edema |
10 (83.3%) |
18 (37.5%) |
0.04[a] |
Near total tumor removal |
10 (83.3%) |
44 (91.6%) |
0.54 |
Postoperative hydrocephalus |
2 (16.6%) |
12 (25%) |
0.67 |
Abbreviation: CMS, cerebellar mutism syndrome.
a Significant.
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Neuroradiographic Features at 1-Year Follow-Up
MRI performed at 1-year follow-up ([Table 3]) of surgery revealed gross atrophy of posterior fossa structures ([Fig. 3C] and [D]), which was more significant in patients with PFS compared with those without this syndrome (p-value = 0.01). There was no significant difference in postoperative shunt required in these patients.
Neuroradiographic features at 1-year follow-up |
CMS present |
CMS absent |
p-Value |
---|---|---|---|
No. of patients |
12 |
48 |
|
Atrophy of posterior fossa structures |
8 (66.6%) |
8 (16.6%) |
0.01[a] |
Presence of shunt |
4 (33.3%) |
8 (29.16%) |
0.84 |
Abbreviation: CMS, cerebellar mutism syndrome.
a Significant.
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Outcome
The GOS at 1-year follow-up ([Table 4]) showed delayed neurological recovery in patients with CMS compared with without CMS.
Abbreviations: CMS, cerebellar mutism syndrome; GOS, Glasgow Outcome Scale.
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Discussion
The incidence of CMS has been reported to range from 2 to 40%.[7] In the largest prospective study so far of 450 children who underwent surgery for medulloblastoma, the incidence of CMS was found to be 24%.[3] In our study, the overall incidence of CMS was found to be 20%, which is concordant with other studies. These variations can be explained by the different definitions of the syndromes (such as PFS and CMS) and the wide spectrum of clinical characteristics. The incidence of CMS was noted to be lower in the past, which might be due to a lack of awareness of this syndrome or even because of difficulty in recalling past events in retrospective studies.[8]
The current study and previous studies showed no association between age and sex at the time of diagnosis and the development of CMS.[5]
The high incidence of CMS in children includes incomplete development of motor speech control and language and the immaturity and incomplete myelination of the reciprocal links in childhood, connecting the cerebellum to the thalamus, sensory areas, motor, and supplementary motor area, making the children more susceptible.[9]
Comparison of various studies on CMS is summarized in [Table 5].
S. No. |
Study |
Journal/year of publication |
Sample size |
Incidence of CMS |
Important findings of the study |
---|---|---|---|---|---|
1. |
Robertson et al[3] |
J Neurosurg/2006 |
450 |
25% |
• Risk factor for CM is brainstem invasion by tumor • One year after diagnosis, nonmotor speech/language deficits, neurocognitive deficits, and/or ataxia persisted in a significant fraction of patients. |
2. |
Wells et al[6] |
J. Neurosurg Paediatr/2010 |
28 |
39% |
• Risk factors for CM are brainstem invasion, and middle and superior cerebellar peduncle edema. • At 1 year postoperatively, patients with CMS showed more moderate to severe atrophy/gliosis of total cerebellum , vermis, and brainstem. • Mean IQ was 16 points lower in patients with CMS compared with those without CMS with a trend toward significance. |
3. |
Küpeli et al[8] |
Pediatr Blood Cancer/2011 |
36 |
25% |
• Risk factors for CM are medulloblastoma histology, midline tumor location of the tumor, and low socioeconomic level of the family. • Intelligence quotients of the patients in PFS and other group with Wechsler Intelligence Scale for Children and the results of the Denver II Developmental Screening Test were not significant statistically. |
4. |
Catsman-Berrevoets and Aarsen[9] |
Cortex/2010 |
148 |
28% |
Duration of mutism correlated with severity of neurological symptoms and abnormalities on SPECT scans of the left temporal lobe, the left and right basal nuclei, and the right frontal lobe. |
5. |
Ozgur et al[17] |
Surg Neurol/2006 |
1 |
100% |
A case is described in which a child exhibiting CM abruptly recovered after the triggering of the melodic speech pathway by way of watching and beginning to sing along with a video. It appears that this incident involving a familiar song catalyzed various speech pathways, which apparently were in some state of shock. |
6. |
Riva and Giorgi[12] |
Brain/2000 |
26 |
Children with right cerebellar tumors presented with disturbances of auditory sequential memory and language processing, whereas those with left cerebellar tumors showed deficits on tests of spatial and visual sequential memory. The vermal lesions led to two profiles: (1) postsurgical mutism and (2) behavioral disturbances. Cerebellum is a modulator of mental and social functions, early in childhood. |
|
7. |
Grill et al[18] |
J Neurosurg/2004 |
76 |
• Risk factors for CM are preoperative HCP incision of the vermis. • Children with cerebellar damage are particularly at risk for long-term neuropsychological dysfunction and require active rehabilitation measures. |
|
8. |
Cobourn et al[19] |
Childs Nerv Syst/2020 |
65 |
10.8% |
• Risk factors for CM are 1 degree of retraction utilized during the procedure and incision of the vermis • Although they did not reach the threshold of statistical significance, tumor vascularity (p = 0.19), adoption of a transvermian approach (p = 0.19), and lack of intraoperative imaging (p = 0.17) exhibited strongly suggestive trends toward a correlation with CMS. |
9. |
Sergeant et al[20] |
J Neurooncol [Internet]/2017 |
22 |
50% |
Risk factors for CM are medulloblastoma, tumor attachment to the floor of the fourth ventricle, calcification/hemosiderin, and postoperative peri-ventricular ischemia on MRI. |
10. |
Pols et al[21] |
J Neurosurg Pediatr/2017 |
71 |
39% |
Risk factors for CM are maximum tumor diameter >5 cm, tumor infiltration or compression of the brainstem, preoperative hydrocephalus, a mean body temperature rise of 0.5°C in the first 4 days after surgery, and increased risk fivefold |
11. |
Setia et al (our study) |
– |
60 |
20% |
• CMS results from transient impairment of the afferent and/or efferent pathways of the dentate nuclei (dentato-thalamo-cortical tract) are involved in initiating complex volitional movements. • Risk factors for CM are brainstem invasion, medulloblastoma histology and midline tumor location, young age, and presence of postoperative brainstem and peduncular edema. • There is delayed neurological recovery in patients with CMS compared with without CMS as shown by Glasgow Outcome Scale (GOS) at 1-year follow-up. • On neurological imaging, patients with CMS show cerebellar peduncular and brainstem edema in immediate post-op and gross atrophy of posterior fossa structures at 1-year follow-up. |
Abbreviations: CM, cerebellar mutism; CMS, cerebellar mutism syndrome; HCP, hydrocephalus; IQ, intelligence quotient; MRI, magnetic resonance imaging; PFS, posterior fossa syndrome.
Pathophysiology
According to Turkstra and Bayles,[10] speech and language production involves five stages: (1) arousal (ascending reticular system); (2) affect and drive (prefrontal and limbic areas); (3) cognition (dominant hemisphere speech areas); (4) initiation, planning, and coordination (Broca's area, supplemental motor area, basal ganglia, thalamus, and cerebellum); and (5) execution (brainstem and cranial nerve nuclei). Research indicates strong reciprocal pathways between the cerebellum and frontal language areas, suggesting that efferent fibers from the dentate nuclei travel through the superior cerebellar peduncle, decussate in the mesencephalic tegmentum, and synapse in thalamic nuclei before projecting to cortical areas.[11]
Most case reports indicate that CMS can follow the resection of midline tumors, typically involving the vermis. Riva and Giorgi[12] noted that vermian lesions may lead to postsurgical mutism, language disorders resembling agrammatism, or behavioral disturbances. However, recent findings suggest that vermis damage may not be as crucial as previously thought, as no correlation was found between vermian tumor location and CMS development. Additionally, many children with posterior fossa tumors undergo radical resection through the vermis without developing CMS, challenging the idea that vermis involvement alone accounts for the syndrome.
The delayed onset of CMS after surgery also weakens the vermis hypothesis. Our study found that while most cases occurred after resection involving the vermis, overall tumor location was not significantly associated with CMS (p = 0.27).
The leading theories regarding CMS pathophysiology involve the dentato-thalamo-cortical (DTC) tract ([Fig. 4]). Mutism can arise from lesions along this tract, particularly during posterior fossa surgery, which often affects its proximal components. Our study showed a significant correlation between preoperative brainstem compression (p = 0.03) and postoperative edema in the superior cerebellar peduncle (p = 0.04) with CMS development. However, identifying dentate nuclei on CT scans proved challenging, and no early MRI was performed during the mutism period.


Cerebello-cerebral diaschisis[13] has also been proposed as a mechanism for CMS, referring to the sudden functional inhibition of brain areas connected to the site of injury. Surgical retraction may cause postoperative edema, disrupting venous circulation and blood supply to the pons through coagulation of perforators from the posterior inferior cerebellar artery.
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Risk Factors
Brainstem involvement, including preoperative tumor invasion or postoperative edema, appears crucial, as our study found brainstem compression to be a significant predictor of cerebellar mutism or CMS (p = 0.03).
Vermian lesions and medulloblastoma histology may be risk factors, as all our cases involved patients with vermian or vermian with lateral extension lesions and none with predominantly hemispheric or brainstem lesions. Most cases (66.6%) had medulloblastoma histology, indicating that midline tumors may pose a higher risk for CMS.
The role of preoperative hydrocephalus as an exacerbating factor for CMS is unclear, as our study found no association (p = 0.45). Additionally, the development of postoperative hydrocephalus and the presence of a shunt at 1 year did not significantly correlate with CMS, consistent with other studies.
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Surgical Aspects
The splitting of the vermis was previously considered a significant factor in the occurrence of CM, leading to efforts to minimize this during surgery. The telovelar approach was initially viewed as a promising technique for posterior cranial tumors. However, Frassanito and Massimi[14] found that it did not significantly prevent CMS in cases involving the cerebellar vermis or brainstem, which are often damaged by the tumor itself. At our institute, the telovelar approach is commonly used, yet 12 cases of CMS were reported, indicating that the surgical approach did not significantly influence CMS prevention. Additionally, near-total tumor removal showed no significant correlation with CMS development (p = 0.54).
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Clinical Presentation
In most cases, symptoms of cerebellar mutism or CM emerged after a period of normal functioning post-surgery, with deficits largely reversible within weeks to months. While mutism is the primary symptom, many patients also exhibited neurological and behavioral issues, including emotional lability, poor oral intake, decreased movement initiation, impaired eye-opening, and oropharyngeal apraxia. These associations were significant (p = 0.005).
Post-mutism dysarthria was notably significant in our population (p < 0.001), suggesting that isolated CM may result from a focal bilateral lesion in the dentate nuclei or their pathways. In contrast, more extensive symptoms, such as oropharyngeal apraxia and global movement impairment, likely indicate broader damage to the para-vermian region and its connections. Ultimately, speech improved in all patients, initially presenting as dysarthric and bizarre but returning nearly to normal.
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Neuroradiographic Features
The presence of brainstem and peduncular edema on immediate postoperative imaging ([Fig. 3B]) significantly correlated with the development of cerebellar mutism or CMS (p = 0.04), suggesting the involvement of the DTC tract. In Robertson et al's[3] study, immediate postoperative MRI showed greater brainstem involvement in CMS patients.
A review of MRI conducted 1-year post-resection revealed significantly more atrophy of posterior fossa structures in CMS patients compared with those without (p = 0.01; [Figs. 3C,D]). This increased atrophy indicates that patients with CMS experienced more persistent damage to the cerebellum, vermis, and brainstem following treatment.
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Outcome
CM was initially viewed as a benign, self-limiting condition, but reports show that some children may still experience mild dysarthria, ataxia, or dysmetria post-resolution. In our study, dysarthria resolved for all patients, while ataxia persisted in four at the 1-year follow-up. Children with cerebellar damage face a high risk of long-term neurophysiological issues, including attention, memory, and behavioral deficits. [Table 4] summarizes GOSs at 1-year follow-up in patients with and without CM.
Robertson et al[3] found a significant link between the initial severity of the syndrome and subsequent ataxia, language dysfunction, and global intellectual impairment. Persistent symptoms can adversely impact a child's language and cognitive development, which is reflected in our findings—no CMS patients achieved a GOS of 1, compared with 10 without CMS.
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Conclusion
CM after posterior fossa tumor surgery is a recognized entity; however, certain issues remain ambiguous regarding the current nomenclature, the exact anatomical substrate, and pathophysiology. The pattern of symptoms ranges from isolated speech impairment to oropharyngeal apraxia to global impairment in initiating volitional activities. In most cases, this syndrome is self-limited, and relatively normal speech is recovered within 3 to 4 months.
The likely substrate for CMS is the DTC tract. The possible risk factors elucidated from our study are the presence of brainstem invasion, medulloblastoma histology, and postoperative brainstem and peduncular edema. The development of CMS after posterior fossa surgery appears to be a “two-hit” phenomenon requiring a combination of existing predisposition, surgical injury, and postoperative exacerbation. Therefore, it is critical to identify the factors involved at each stage and investigate treatments to target them appropriately. Advanced imaging techniques can help to identify possible preoperative risk factors. Selection of the less hazardous surgical approaches (Telovelar) could be achieved. Proper counseling of caregivers is essential in these cases for the potential sequelae and possible outcomes.
It should be emphasized that the overall cognitive outcome of this syndrome is not as favorable as previously thought[15] [16] and that periodical neurocognitive assessments of such patients—especially of younger age, with malignancy, and potentiality for radiation therapy—should be considered. A degree of reduced risk for CMS may come with further clarification of the anatomical milieu of posterior fossa brain tumors.
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Conflict of Interest
None declared.
Ethical Approval
The study has been approved by the Ethics Committee of Maulana Azad Medical College, New Delhi, India.
Patients' Consent
All participants gave written informed consent to participate prior to enrolment in the study.
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Artikel online veröffentlicht:
13. Januar 2025
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