This very recent (May 2022) review was posted elsewhere (FB) and after reading it myself (it's open access) I thought it worth re-posting here on HU - for those interested in learning more on long-term DBS outcomes.
movementdisorders.onlinelib...
… excerpts from their conclusion
“The introduction of STN-DBS by Benabid and Pollak in the early 1990s clearly marks the second major breakthrough in the symptomatic treatment of PD after the discovery of levodopa in the 1960s. Since then, many RCTs and a growing body of observational evidence have established the profound and long-lasting symptomatic effects of DBS for 10 years and longer. Therefore, DBS has clearly has made an impact on the course of PD, not only by substantially diminishing levodopa induced motor complications, but also by providing relief for those with drug-refractory tremor. These effects and the resultant improvements in QoL and ADLs, however, start to decline around 5 years into DBS treatment as disease progression begins to catch up. Although motor symptoms including tremor and bradykinesia are well-controlled by DBS for 10 years or longer, axial motor symptoms like gait impairment, freezing of gait, and dysarthria worsen and, along with bothersome non-motor symptoms such as psychosis, dementia, and dysautonomia dominate the clinical picture seen in patients with very long-term DBS.”
“Whether DBS is able to delay such major disease milestones or modify the progression of the disease is difficult to answer from currently published observational studies because of their heterogenous and mainly non-controlled designs. Nonetheless, there are signals from studies comparing DBS treated patients with retrospectively constructed control PD populations suggesting that chronic subthalamic DBS may lower the risk for or delay some important disability milestones such as falls, psychosis, and need for long-term care and may be associated with slightly prolonged survival. Reasons behind this may relate to the long-term control of motor complications and reductions in medication-induced side effects, which lead to improved mobility, personal care, and general health, rather than to a true “disease-modifying” effect. “
“Meanwhile, technological developments are rapidly advancing and enabling new neurostimulation approaches. Examples include directional electrodes, artificial intelligence and imaging-based programming, and adaptive and closed-loop stimulation, that are aimed at further refining stimulation toward personalized treatment and will assist clinicians to deal with increasingly complex programming features. For patients already under DBS, strategies to improve outcomes are also being investigated. One example are axial motor symptoms such as gait impairment and freezing of gait for which low frequency stimulation, drugs (eg, rivastigmine), or physiotherapy may provide relief.
Therefore, DBS will continue to evolve, leading toward enhanced efficacy and safety. The latter issues are what matter most to patients and even if DBS does not ultimately prevent progressive disability, it continues to substantially change the outlook for many people with PD, whose function and QoL has become compromised by motor complications.”