Bridging the Gap: Neurocircuitry Behind Mutism: Insights From a Midbrain Lesion.

Abstract

Acquired mutism, including akinetic mutism (AM) and postoperative pediatric cerebellar mutism syndrome (ppCMS), arises from damage to specific brain regions and is characterized by an inability to produce verbal communication. AM is associated with damage to fronto-subcortical motivational circuits and-in addition to mutism-presents with akinesia, whereas ppCMS involves disruption of (non)motor cerebello-cerebral circuits and is further characterized by emotional lability and a typically delayed onset. We report a case of a 10-year-old patient who developed mutism after surgical resection of a suprasellar craniopharyngioma complicated by a focal ischemic lesion in the midbrain. Postoperatively, the patient experienced progressive loss of speech and voluntary motor functions beginning on day 5 and culminating in mutism and akinesia on day 12. In the absence of spontaneous recovery, treatment with methylphenidate was initiated, after which the patient demonstrated gradual improvement, regaining speech and showing continued recovery of motor deficits up to 4 months after the ischemic event. This case highlights overlap between AM and ppCMS features, raising the possibility that these entities may represent a disease spectrum, driven by disruptions in specific neurocircuits. The neurocircuits involved in AM and ppCMS intersect at the level of the midbrain (presented in Graphical Abstract for visualization). We hypothesize that the co-occurrence of clinical features of both AM and ppCMS reflects disruption of overlapping neurocircuitry at the midbrain level.