CarolineMoreau, Department of Neurology and Movement Disorders, EA2683, IFR 114, University of Lille 2, Clinique Neurologique, Hôpital R. Salengro, CHU, F-59037 LILLE cedex FRANCEc-moreau@chru-lille.fr
Luc Defebvre, Alain Destée, Séverine Bleuse, Frédérik Clement, Jean-Louis Blatt, Pierre Krystkowiak and David Devos
Submitted June 26, 2008
We thank Dr. Brozova and colleagues for their comments on our article and their findings which underline the utility of investigating modulation of STN DBS parameters in general and the stimulation frequency in particular.
The idea of increasing voltage in order to obtain a better efficacy is partially true and somewhat limited. The effects of DBS remain unclear and inconsistent. [4] It is evident that the neurodegeneration and disease progression modify the various brain structures involved [5] and thus their activity. This has led to the concept of different disease phenotypes within PD. These phenotypes could be associated with different patterns of noisy basal ganglia signals that disrupt both local and remote functions. [5]
In addition to the hypothetical diffusion of current to the PPN, it has been suggested that different DBS frequencies may suppress or override the various noisy signals in the basal ganglia-cortical loop (i.e. in the beta band, <30 Hz). [6] Or, they may boost disease-impaired local activity in these structures (i.e. in the gamma band, 60-90 Hz). The clinical results confirm fundamental studies suggesting that DBS not only suppresses the abnormal pattern of basal ganglia activity but also drives activity that mimics normal gamma band patterns (60 Hz).
The current challenge is to define the various frequency effects for different phenotypes and candidates. This is in progress for gait disorders but speech disturbances and cognitive functions require further investigation. Our initial results suggest that good candidates for 60Hz STN DBS may be PD patients with: long disease duration; severe gait disorders with freezing of gait; and predominant but partially dopa-responsive axial signs. However, these findings need further confirmation.
Finally, to improve the benefit of 60Hz STN DBS, it may be necessary to increase the voltage at 60 Hz within a range that could vary among patients. Voltage should be assessed stepwise in each patient from 4 to 5.5V. In addition, the range could be higher than the previously reported increase of 1.3 V (range: 0.7- 2.5).
With 60 Hz and a 60 µs pulse width, we observed a greater improvement in gait at 5V than at 4V. [1]
References
4. Brown and Eusebio. Paradoxes of Functional Neurosurgery: clues from basal ganglia recordings. Mov Disorders 2008;23:12-20.
5. Braak H, Ghebremedhin E, Rub U, Bratzke H, Del Tredici K. Stages in the development of Parkinson's disease-related pathology. Cell Tissue Res. 2004;318:121-134.
6. Devos D, Szurhaj W, Reyns N et al Predominance of the contralateral movement-related activity in the subthalamo-cortical loop. Clinical Neurophysiology 2006;117 :2315-2327.
Disclosure: The authors report no conflicts of interest.
We thank Dr. Brozova and colleagues for their comments on our article and their findings which underline the utility of investigating modulation of STN DBS parameters in general and the stimulation frequency in particular.
The idea of increasing voltage in order to obtain a better efficacy is partially true and somewhat limited. The effects of DBS remain unclear and inconsistent. [4] It is evident that the neurodegeneration and disease progression modify the various brain structures involved [5] and thus their activity. This has led to the concept of different disease phenotypes within PD. These phenotypes could be associated with different patterns of noisy basal ganglia signals that disrupt both local and remote functions. [5]
In addition to the hypothetical diffusion of current to the PPN, it has been suggested that different DBS frequencies may suppress or override the various noisy signals in the basal ganglia-cortical loop (i.e. in the beta band, <30 Hz). [6] Or, they may boost disease-impaired local activity in these structures (i.e. in the gamma band, 60-90 Hz). The clinical results confirm fundamental studies suggesting that DBS not only suppresses the abnormal pattern of basal ganglia activity but also drives activity that mimics normal gamma band patterns (60 Hz).
The current challenge is to define the various frequency effects for different phenotypes and candidates. This is in progress for gait disorders but speech disturbances and cognitive functions require further investigation. Our initial results suggest that good candidates for 60Hz STN DBS may be PD patients with: long disease duration; severe gait disorders with freezing of gait; and predominant but partially dopa-responsive axial signs. However, these findings need further confirmation.
Finally, to improve the benefit of 60Hz STN DBS, it may be necessary to increase the voltage at 60 Hz within a range that could vary among patients. Voltage should be assessed stepwise in each patient from 4 to 5.5V. In addition, the range could be higher than the previously reported increase of 1.3 V (range: 0.7- 2.5).
With 60 Hz and a 60 µs pulse width, we observed a greater improvement in gait at 5V than at 4V. [1]
References
4. Brown and Eusebio. Paradoxes of Functional Neurosurgery: clues from basal ganglia recordings. Mov Disorders 2008;23:12-20.
5. Braak H, Ghebremedhin E, Rub U, Bratzke H, Del Tredici K. Stages in the development of Parkinson's disease-related pathology. Cell Tissue Res. 2004;318:121-134.
6. Devos D, Szurhaj W, Reyns N et al Predominance of the contralateral movement-related activity in the subthalamo-cortical loop. Clinical Neurophysiology 2006;117 :2315-2327.
Disclosure: The authors report no conflicts of interest.