Session Information
Date: Monday, June 20, 2016
Session Title: Surgical therapy: Parkinson's disease
Session Time: 12:30pm-2:00pm
Location: Exhibit Hall located in Hall B, Level 2
Objective: Deep brain stimulation (DBS) of the pedunculopontine nucleus (PPN) has been reported to improve motor symptoms in idiopathic (IPS) and in atypical Parkinsonian syndromes (APS). We here report our clinical experiences of 11 cases with Parkinsonian syndromes during a follow-up of 24 month.
Background: The PPN forms a crucial relay between the basal ganglia and the spinal cord motor systems. Low frequency stimulation of that target has influence on gait and postural reflexes. These axial motor symptoms are often resistant to levodopa treatment.
Methods: 11 Patients (4 male, 7 female, age range 56-74 years, disease duration 2-14 years) with Parkinsonian syndromes were treated by PPN DBS for severe gait and balance disorder. Three patients met clinical criteria of an IPS. Eight patients were classified as APS (7 PSP, 1 MSA). Five patients received DBS of an additionally target (4x bilateral subthalamic nucleus, 1x bilateral internal globus pallidus). Clinical evaluation included history, motor scales (UPDRS motor scale, Tinetti gait test and “timed up and go”- test), automated gait analysis and posturography in DBS on/off-state with different frequencies (8, 20, 60, 130 Hz), and cognitive examination. Clinical follow-up was at 12 month in all cases and at 24 month in 7 cases. Patient and clinical examiner were blinded for DBS condition.
Results: PPN DBS showed no significant effect on clinical motor scores. The automated gait analysis revealed a significant improvement of cadence and stride time during stimulation with 60 Hz, but not for other gait and balance parameters.
Conclusions: Contrary to previous clinical reports our present data do not support the PPN as a valuable target in treatment of levodopa resistant axial symptoms in Parkinsonian disorders, especially in patients with atypical Parkinsonian syndromes. The progressive midbrain atrophy and succeeding changes in PPN physiology might be might be one reason of the therapeutic failure in these patients.
To cite this abstract in AMA style:
I. Galazky, A. Kupsch, E. Wirkus, F. Casjens, S. Specht, H.J. Heinze, J. Voges. Is the PPN a valuable target for deep brain stimulation in treatment of Parkinsonian disorders? Experience of a patient’s series [abstract]. Mov Disord. 2016; 31 (suppl 2). https://www.mdsabstracts.org/abstract/is-the-ppn-a-valuable-target-for-deep-brain-stimulation-in-treatment-of-parkinsonian-disorders-experience-of-a-patients-series/. Accessed June 14, 2025.« Back to 2016 International Congress
MDS Abstracts - https://www.mdsabstracts.org/abstract/is-the-ppn-a-valuable-target-for-deep-brain-stimulation-in-treatment-of-parkinsonian-disorders-experience-of-a-patients-series/