Late-Onset Ataxia after Thalamic Deep Brain Stimulation for Tremor Linked to Therapy Escape

Thalamic ventral intermediate nucleus (VIM) deep brain stimulation (DBS) is a well-established treatment for pharmacoresistant tremor. Tremor habituation is reported in 0% to 73.3% of patients. Some adverse events such as late-onset ataxia result several years after DBS, and little is known about the risk factors.

We developed a retrospective study to highlight the predictors for onset of ataxia in patients treated with DBS of the VIM for pharmacoresistant tremor and its possible connection to DBS habituation.

We conducted an observational, retrospective, and monocentric study in Nice University Hospital, including all patients treated with VIM DBS for refractory tremor due to essential tremor, Parkinson's disease, and other pathologies. We collected data regarding DBS parameters, tremor etiology, ataxia onset, and DBS habituation.

Among 61 patients, 30 developed ataxia within a mean of 36.03 months (±15.57) after surgery. The number of modifications of DBS settings during the first year (0.931 vs. 2.0, P = 0.01) and after the first year (2.0 vs. 4.84, P < 0.001) and tremor habituation (7.14% vs. 44.83%, P = 0.002) are significantly higher in the ataxic group. The discontinuation of stimulation at nighttime is significantly correlated to less ataxia (37.93% vs. 13.33%, P = 0.039).

We highlighted a strong statistical relationship between ataxia and habituation, suggesting they might be 2 expressions of the same phenomenon. The patients developing late ataxia seem to be those presenting with an early habituation as early as in the first year. Our series demonstrates that intermittent stimulation might be a protecting factor from late ataxia.