Abstract

Subthalamic deep brain stimulation (STN DBS) for Parkinson's disease typically enables a 50% reduction in dopaminergic medication postoperatively. This reduction in medication is accompanied by a 60% reduction in dyskinesia and a reduction in off periods. However, there remains a subgroup of patients who have disabling dyskinesias despite optimisation of drug and stimulator setting. Amantadine is sometimes used for the medical management of drug-induced dyskinesias in Parkinson's disease. Its use in dyskinesias after DBS has not been formally assessed.

We report a series of 8 cases who had bilateral STN DBS. These patients had similar characteristics to our local database of patients who have had DBS. However, these patients had disabling bradykinesia and/or dyskinesias despite attempts at optimisation of stimulator settings and dopaminergic medication. The addition of amantadine led to clear improvements in dsykinesias and/or mobility, without the need to increase the total dose of dopaminergic medication. Stopping amantadine caused worsening of symptoms.

This case series suggests amantadine is an important additional medication in the small group of patients whose disease has not been stabilised after DBS. The outflow of the STN includes a glutamatergic pathway. The glutamate receptor blocking properties of amantadine provide a possible mechanism for the observed benefit.

We plan to extend the results of this case series to include objective scoring in subsequent patients.