Dopamine reverses reward insensitivity in apathy following globus pallidus lesions.
Level 4 - case-series / case-control
Case report of a single patient with focal basal ganglia lesions
PubMed 22721958 · doi:10.1016/j.cortex.2012.04.013
What was done
Researchers evaluated a single patient who developed profound apathy following bilateral focal lesions of the basal ganglia, specifically affecting globus pallidus regions connected to the orbitofrontal and ventromedial prefrontal cortex. The investigators assessed the patient's reward sensitivity using two oculomotor decision-making tasks under baseline conditions and after administration of levodopa or a dopamine receptor agonist, alongside clinical assessments of apathy, motivation, and social interaction.
What was found
The abstract does not report numerical data, effect sizes, or test statistics. Qualitatively, the patient exhibited reward insensitivity on oculomotor decision-making tasks at baseline. Reward sensitivity was partially re-established with levodopa and more effectively with a dopamine receptor agonist. These changes were accompanied by clinical improvement, including reduced apathy, greater motivation, and increased social interactions.
Why it matters
This study provides mechanistic evidence that reward insensitivity from globus pallidus circuit dysfunction contributes to pathological apathy and can be reversed pharmacologically with dopaminergic agents.
Limits
The findings derive from a single patient (n=1) without a control comparator, limiting generalizability to wider neurodegenerative populations. The abstract does not report quantitative task metrics, drug dosages, or assessment timeframes.
Cited by
- supports In a case of pathological apathy caused by bilateral basal ganglia strokes, the dopamine agonist ropinirole restored motivated behavior after levodopa had failed.