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ObjectiveTo evaluate the effectiveness of levodopa‐carbidopa intestinal gel (LCIG) as an add‐on rescue therapy following deep brain stimulation (DBS) for treatment of motor fluctuations.BackgroundBoth DBS and LCIG are FDA‐approved therapies for treatment of motor fluctuations in advanced PD. Few studies have examined dual therapy for refractory motor fluctuations and it is unknown what the effect on quality of life will be in advanced PD.MethodsWe conducted a retrospective study using a large database of all medical and surgical PD cases at the University of Florida. Six patients were identified with DBS who subsequently received rescue LCIG therapy. The clinical histories, indications for intervention and outcomes were reviewed.ResultsAll patients were managed initially with DBS (bilateral STN DBS (n = 3), bilateral GPi DBS (n = 1), unilateral GPI DBS (n = 2)). Patients with well‐placed (n = 3) and suboptimally placed DBS leads (n = 3) had significant reduction in their motor fluctuations with improvement in the off‐medication time after rescue LCIG therapy. Improvement in quality of life scores (PDQ‐39) was appreciated in four DBS patients following the addition of LCIG therapy.ConclusionsLCIG is a promising add‐on rescue therapy for select patients with existing DBS devices. The LCIG may possibly reduce motor fluctuations and improve quality of life in advanced PD irrespective of the DBS target or the accuracy of lead placement. Dual therapy may also be ideal for patients who are considered high risk for additional DBS surgeries.

This study revealed that approximately three out of four post-mortem DBS cases exhibited pathological evidence of a glial collar or scar present at the ventral DBS lead tip. The amount of gliosis was not significantly associated with duration of DBS. Future studies should include serial sectioning across all DBS contacts with correlation to the volume of tissue activation and to the clinical outcome.

Objectives The aim of this study is to identify anatomical regions related to stimulation‐induced dyskinesia (SID) after pallidal deep brain stimulation (DBS) in Parkinson's disease (PD) patients and to analyze connectivity associated with SID. Methods This retrospective study analyzed the clinical and imaging data of PD patients who experienced SID during the monopolar review after pallidal DBS. We analyzed structural and functional connectivity using normative connectivity data with the volume of tissue activated (VTA) modeling. Each contact was assigned to either that producing SID (SID VTA) or that without SID (non‐SID VTA). Structural and functional connectivity was compared between SID and non‐SID VTAs. “Optimized VTAs” were also estimated using the DBS settings at 6 months after implantation. Results Of the 68 consecutive PD patients who underwent pallidal implantation, 20 patients (29%) experienced SID. SID VTAs were located more dorsally and anteriorly compared with non‐SID and optimized VTAs and were primarily in the dorsal globus pallidus internus (GPi) and dorsal globus pallidus externus (GPe). SID VTAs showed significantly higher structural connectivity than non‐SID VTAs to the associative cortex and supplementary motor area/premotor cortex (P < 0.0001). Simultaneously, non‐SID VTAs showed greater connectivity to the primary sensory cortex, cerebellum, subthalamic nucleus, and motor thalamus (all P < 0.0004). Functional connectivity analysis showed significant differences between SID and non‐SID VTAs in multiple regions, including the primary motor, premotor, and prefrontal cortices and cerebellum. Conclusion SID VTAs were primarily in the dorsal GPi/GPe. The connectivity difference between the motor‐related cortices and subcortical regions may explain the presence and absence of SID. © 2020 International Parkinson and Movement Disorder Society

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Clinical vignette A 68-year-old male with a 16-year history of Parkinson's disease (PD) underwent bilateral globus pallidus internus (GPi) deep brain stimulation (DBS) at the University of Florida. He was treated with DBS for the management of motor fluctuations, levodopa-induced dyskinesia (LID), and dystonia. Surgery was performed with microelectrode recording (MER) guidance. During the initial postoperative monopolar threshold review (Table 1), he developed stimulation-induced dyskinesia (SID) in the right hemibody with monopolar activation of the dorsal contacts (contacts 2 and 3) of the left GPi lead. No SID was noted with the stimulation of the ventral contacts (contacts 0 and 1) of the left GPi lead or with the stimulation of any of the contacts of the right GPi lead. Contact 1 stimulation on the left DBS lead provided benefit for tremor, bradykinesia, and rigidity. Contact 2 provided a more robust improvement in bradykinesia and rigidity but the benefit was limited by SID. Postoperative lead localization and three-dimensional (3D) mapping identified that both leads were appropriately placed in the posterolatero-ventral GPi (Figure 1). Contact 2 is located in the dorsal GPi/GPe area and contact 3 is located in the GPe area. Clinical dilemma This case represents dorsal GPi and GPe SID in a patient with PD. On the left GPi DBS lead, contacts 1 and 2 provided the best clinical benefit. Contact 1 monopolar stimulation improved the tremor but did not have a robust effect on bradykinesia and rigidity. Contact 2 stimulation on the other hand, improved tremor, rigidity, and bradykinesia, but the benefit

BackgroundPure akinesia with gait freezing is a rare syndrome with few autopsied cases. Severe freezing of gait occurs in the absence of bradykinesia and rigidity. Most autopsies have revealed progressive supranuclear palsy. We report the clinical and postmortem findings of two patients with pure akinesia with gait freezing, provide video recordings of these patients, and review the literature describing similar cases. We also discuss bradykinesia, hypokinesia and akinesia in the context of this clinical syndrome.Case presentationTwo patients with the syndrome of pure akinesia with gait freezing were examined by the same movement disorder specialist at least annually for 9 and 18 years. Both patients initially exhibited freezing, tachyphemia, micrographia and festination without bradykinesia and rigidity. Both autopsies revealed characteristic tau pathology of progressive supranuclear palsy, with nearly total neuronal loss and gliosis in the subthalamus and severe neuronal loss and gliosis in the globus pallidus and substantia nigra. Previously published postmortem studies revealed that most patients with this syndrome had progressive supranuclear palsy or pallidonigroluysian atrophy.ConclusionsPallidonigroluysian degeneration produces freezing and festination in the absence of generalized slowing (bradykinesia). Freezing and festination are commonly regarded as features of akinesia. Akinesia literally means absence of movement, and akinesia is commonly viewed as an extreme of bradykinesia. The pure akinesia with gait freezing phenotype illustrates that bradykinesia and akinesia should be viewed as separate phenomena.Electronic supplementary materialThe online version of this article (doi:10.1186/s40734-017-0063-1) contains supplementary material, which is available to authorized users.

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