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Background And Objectives: Despite the well-established efficacy of deep brain stimulation (DBS) of the subthalamic nucleus (STN) for Parkinson's Disease (PD), there remains a subset of patients with only a moderate improvement in symptoms even with appropriate lead placement and optimal programming. In patients with persistent tremor or dyskinesias, one consideration is the addition of a second "rescue lead" to provide dual stimulation to primary and secondary targets to address the refractory component. This study aimed to assess all "rescue lead" cases from our institution and characterize the patients and their outcomes.
Methods: Records of all patients with PD treated at our institution between 2005 and 2023 were retrospectively reviewed. Clinical data of all patients treated with a second rescue lead to supplement a positive but inadequate initial DBS response were collected and reviewed.
Results: Of 670 patients with PD treated at our institution during the study period, 7 were managed with a rescue lead. All 7 were initially treated with STN DBS with a partial improvement in underlying symptoms, had confirmed appropriate lead placement, and underwent thorough programming. Four patients underwent rescue with a globus pallidus interna lead for persistent dyskinesias, all with subsequent improvement in their dyskinesias. Three patients had persistent tremors that were treated with a rescue ventrointermediate thalamus stimulation with subsequent improvement in tremor scores. There were no operative complications, and all patients tolerated dual stimulation.
Conclusion: For a small subset of patients with PD with persistent dyskinesias or tremors after STN DBS despite optimized lead parameters and adequate lead placement, rescue lead placement offers an effective treatment option.
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http://dx.doi.org/10.1227/ons.0000000000001142 | DOI Listing |
Neurobiol Dis
September 2025
University of Nebraska Medical Center, College of Medicine, Department of Neurological Sciences, Omaha, NE, USA. Electronic address:
Amongst the major histopathological hallmarks in Alzheimer's disease are intracellular neurofibrillary tangles consisting of hyperphosphorylated and aggregated Tau, synaptic dysfunction, and synapse loss. We have previously shown evidence of synaptic mitochondrial dysfunction in a mouse model of Tauopathy that overexpresses human Tau (hTau). Here, we questioned whether the levels or activity of Parkin, an E3 ubiquitin ligase involved in mitophagy, can influence Tau-induced synaptic mitochondrial dysfunction.
View Article and Find Full Text PDFCell Rep
August 2025
Laboratory of Animal Resources, Center for Disease Biology and Integrative Medicine, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan. Electronic address:
Fragile X syndrome (FXS) is the foremost monogenic cause of autism spectrum disorder and intellectual disability, caused by FMR1 gene silencing. Here, we report that common marmosets carrying FMR1 mutation, a non-human primate model for FXS, share common features in behavioral and molecular phenotypes with patients with FXS. Founder mutants with markedly reduced fragile X messenger ribonucleoprotein expression display hyperactivity, spontaneous seizures, and transcriptome changes in synapse-related genes that overlap with those reported in patients with FXS.
View Article and Find Full Text PDFJ Neurosci
September 2025
Center for Neurodegenerative Disease Research, Dept. Pathology, Perelman School of Medicine at the University of Pennsylvania, 3 Maloney Bldg, 3600 Spruce St, Philadelphia, PA 19140, USA.
Neuronal hyperexcitability is a hallmark of amyotrophic lateral sclerosis (ALS) but its relationship with the TDP-43 aggregates that comprise the predominant pathology in over 90% of ALS cases remains unclear. Emerging evidence indicates that TDP-43 pathology induces neuronal hyperexcitability, which may contribute to excitotoxic neuronal death. To characterize TDP-43 mediated network excitability changes in a disease-relevant model, we performed in vivo continuous electroencephalography monitoring and ex vivo acute hippocampal slice electrophysiology in rNLS8 mice (males and females), which express human TDP-43 with a defective nuclear localization signal (hTDP-43ΔNLS).
View Article and Find Full Text PDFFront Med (Lausanne)
August 2025
Suzhou Medical College of Soochow University, Soochow, Jiangsu, China.
Introduction: Emergence agitation (EA) is a common postoperative complication characterized by confusion, disorientation, and restless behavior that can lead to self-harm, the removal of medical devices, and other adverse events. This randomized, double-blind, placebo-controlled study was designed to assess the efficacy and safety of a novel benzodiazepine, remimazolam, in the management of EA.
Methods: A total of 219 adults experienced EA (Riker Sedation-Agitation Scale SAS score ≥5) after otolaryngological surgery were randomly assigned (1:1:1 ratio) to receive one of the following three treatments: 2.
Mol Ther Nucleic Acids
September 2025
Molecular Cardiology Laboratory, IRCCS Policlinico San Donato, San Donato Milanese, Milan 20097, Italy.
Myotonic dystrophy type 1 (DM1) is a multisystemic disorder caused by expanded CTG repeats in the 3'-UTR of the gene that lead to nuclear foci accumulation and splicing defects. Circular RNAs (circRNAs) are emerging regulators of muscular disorders, but their role in DM1 remains largely unknown. By analyzing available RNA-sequencing datasets from DM1 patients, followed by validation in patients and matching control muscle biopsies, we identified seven circRNAs that were significantly increased in DM1 muscles and displayed high circular-to-linear isoform ratios.
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