Non-Surgical Cerebellar Mutism Syndrome

Background: Cerebellar Mutism Syndrome (CMS), also termed Posterior Fossa Syndrome, is characterised by mutism, ataxia, and emotional lability, with variable recovery and potential long-term sequelae. While posterior fossa tumor resection in children is a known cause of CMS, non-surgical cases have been reported in association with infection, inflammation, and vascular, traumatic, and metabolic cerebellar insults. Recognition of this entity is important, as it expands the spectrum of CMS beyond postoperative cases and deepens our insight into the cerebellum’s contributions to speech, motor, and cognitive functions. Case Presentation Summary: Case 1: A 10-year-old boy presented with a short history of headache, vomiting, and lethargy, progressing to mutism, severe ataxia, hypotonia, and dysmetria. MRI demonstrated diffuse cerebellitis and leptomeningeal enhancement. Despite treatment with corticosteroids, intravenous immunoglobulin, and plasma exchange, recovery was protracted, requiring intensive multidisciplinary rehabilitation. Gross motor function improved first, followed by fine motor skills and speech. By seven months, balance and speech had returned to baseline, though fine motor coordination remained limited. Case 2: A 4-year-old girl presented with fever, abdominal pain, vomiting, irritability, and lethargy, progressing to mutism, ataxia, dysmetria, dystonic posturing and reduced GCS. She tested positive for Influenza A (H1) and MRI confirmed diffuse cerebellitis. She received intravenous methylprednisolone, oseltamivir, and supportive therapies. Gradual recovery followed, with vocalisation returning by day 18 of admission and significant improvements in motor and language function by discharge. At three months, she had fully regained her baseline gross and fine motor abilities and speech. Both children achieved near-complete functional and speech recovery with intensive multidisciplinary input, though subtle fine motor difficulties persisted in case 1. Learning Points Discussion: These cases highlight that CMS can arise independently of surgical intervention, underscoring the importance of recognising cerebellar pathology as a cause of acute mutism in children. The clinical picture parallels postoperative CMS, with delayed-onset mutism, emotional lability, ataxia, followed by staged recovery of motor and speech functions. MRI supported cerebellar involvement, and both patients benefited from multidisciplinary rehabilitation, with music therapy playing a particularly meaningful role in the first case. Recovery trajectories varied, with potential for persistent fine motor deficits despite resolution of speech impairment. Literature review confirms multiple infectious and inflammatory causes, with rotavirus, influenza, and autoimmune conditions, such as acute disseminated encephalomyelitis (ADEM) and MOG-associated disease, as recurring aetiologies. Proposed mechanisms include functional disruption of the dentato-thalamo-cortical network, diaschisis, and involvement of the fastigial nuclei and ventral periaqueductal grey. These cases add to the limited but growing body of evidence on non-surgical CMS, emphasising the cerebellum’s integral role in motor, speech, and emotional regulation. Clinicians should consider CMS in children presenting with acute mutism and cerebellar signs, even in the absence of neurosurgical history. Early recognition and comprehensive rehabilitation, including speech, occupational, physiotherapy, and adjunctive music therapy, are essential for optimizing recovery.