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Published on: November 17, 2021
Pathological laughter and behavioural change in childhood pontine glioma
Darren R Hargrave1, Donald J Mabbott, Eric Bouffet
1Paediatric Oncology Unit, Royal Marsden Hospital, Downs Road, SM2 5PT, Sutton, Surrey, UK. darren.hargrave@rmh.nhs.uk
Insights
Pontine glioma in children can cause unusual behavioral changes like pathological laughter or separation anxiety, challenging the view of the pons as solely mediating motor functions. This suggests a broader role for the pons in affective behavior through disrupted brain networks.
Area of Science:
- Pediatric Neurology
- Neuro-oncology
- Behavioral Neuroscience
Background:
- Pontine glioma is typically associated with motor deficits and cranial nerve palsies.
- The pons has not traditionally been recognized for its role in complex affective behaviors.
Observation:
- Nine children with pontine glioma exhibited significant behavioral changes.
- These changes included pathological laughter and separation anxiety (school refusal).
Findings:
- Pontine lesions can disrupt cerebro-ponto-cerebellar pathways.
- This disruption may underlie the observed complex affective and cognitive behavioral changes.
Implications:
- The pons may play a more significant role in affective behavior than previously understood.
- Understanding these pathways is crucial for diagnosing and managing pontine glioma.
- This research opens new avenues for studying brain-behavior relationships in pediatric neuro-oncology.
Abstract:
Children with pontine glioma usually present classically with ataxia, motor deficits and cranial nerve palsies. The pons has generally not been regarded as a structure that mediates complex affective behaviour. However, we report nine children who either at the time of presentation or progression demonstrated marked behavioural changes manifesting as either "pathological laughter" or separation anxiety in the form of school refusal. A mechanism of how pontine lesions can cause such complex affective and cognitive behaviour has been suggested to consist of the disruption of a network of cerebro-ponto-cerebellar pathways and the evidence for this mechanism is discussed.
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