A Case of Acute-Onset, Refractory Freezing of Gait Following Subthalamic Nucleus Deep Brain Stimulation Adjustment

Freezing of gait (FoG) is a disabling symptom of Parkinson's disease (PD) characterized by involuntary cessation/reduction. While deep brain stimulation (DBS) targeting the subthalamic nucleus (STN) effectively treats common PD symptoms such as tremor, its impact on FoG is less clear. Rarely, STN-DBS itself can induce FoG. Reversible cases have been linked to hyperdopaminergic states, high-frequency stimulation, and suboptimal DBS lead placement. One irreversible case occurred immediately after DBS surgery and was attributed to lesioning of gait pathways during lead insertion. We report a case of seemingly irreversible FoG that began not after lead insertion or initial activation, but after initial follow-up adjustment in STN-DBS with otherwise proper placement and expected benefit. A 62-year-old female underwent STN-DBS for medication-resistant symptoms of idiopathic PD. The leads were activated at 125 Hz without adverse events. The patient returned two weeks later for stimulation adjustment. Two days after that visit, the patient developed severe FoG, resulting in falls. Despite many adjustments to both stimulation parameters and medications, the patient continued to experience FoG even with the device off. Lower frequency stimulation (55 Hz) provided partial, temporary improvement in FoG. Low-frequency parameters and off-stimulation trials were limited by the patient's severe dystonia. Spatial reconstruction confirmed the active contacts were within the STN. This timeline of events differs from previously reported cases attributed to anatomic/structural causes (lead mispositioning vs. gait pathway lesioning), hyperdopaminergic states, or high-frequency stimulation. Although the utilized contacts appear to be appropriately positioned, iatrogenic induction of FoG is too poorly understood to exclude their position as a factor. This case could be explained as a combination of positional- and frequency-induced FoG if not for the persistence of FoG when off-stimulation. It is possible that the "off trials" were not long enough for the adverse effects of stimulation to fully subside. Longer "off trials" are limited by the patient's severe dystonia. Post-STN-DBS FoG refractory to stimulus on/off state is a rare phenomenon reported only twice in the current literature (including this case). The current report describes the first patient for whom significantly refractory FoG specifically began after stimulus adjustment; this may represent lasting negative effects of stimulation in the DBS "off" state. Comprehensive reporting of anatomical lead locations and stimulation parameters in similar cases is essential to identify patterns that could inform future interventions.