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Bridging the Gap: Neurocircuitry Behind Mutism: Insights From a Midbrain Lesion
Iris V Obdeijn1, Eveline J Langereis2, Mylène C Berk3
1Research Department, Princess Máxima Center for Pediatric Oncology, Utrecht, the Netherlands.
Neurology
|July 27, 2026
Summary
A 10-year-old patient developed acquired mutism and akinesia after brain surgery. Methylphenidate treatment led to speech and motor recovery, suggesting a spectrum of mutism disorders possibly linked to midbrain circuitry.
Area of Science:
- Neuroscience
- Pediatric Neurology
- Neurosurgery
Background:
- Acquired mutism, including akinetic mutism (AM) and postoperative pediatric cerebellar mutism syndrome (ppCMS), results from specific brain damage.
- AM involves fronto-subcortical circuits, causing mutism and akinesia.
- ppCMS affects cerebello-cerebral circuits, leading to emotional lability and delayed onset.
Purpose of the Study:
- To report a case of acquired mutism following brain surgery.
- To explore the relationship between AM and ppCMS.
- To investigate the role of midbrain circuitry in these conditions.
Main Methods:
- Case report of a 10-year-old patient with a suprasellar craniopharyngioma.
- Analysis of postoperative neurological deficits including mutism and akinesia.
- Treatment with methylphenidate and monitoring of recovery.
Main Results:
- The patient developed mutism and akinesia 5-12 days post-surgery due to a midbrain ischemic lesion.
- Methylphenidate treatment resulted in gradual recovery of speech and motor functions.
- Clinical presentation showed overlap between AM and ppCMS features.
Conclusions:
- The case suggests AM and ppCMS may represent a disease spectrum due to disrupted neurocircuitry.
- Overlapping features indicate shared or intersecting neurocircuitry at the midbrain level.
- Midbrain circuitry disruption is hypothesized to cause the co-occurrence of AM and ppCMS clinical features.
