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Cognitive impairment is the most frequent non-motor symptom in Parkinson's disease and is associated with deficits in a number of cognitive functions including working memory. However, the pathophysiology of Parkinson's disease cognitive impairment is poorly understood. Beta oscillations have previously been shown to play an important role in cognitive functions including working memory encoding. Decreased dopamine in motor cortico-striato-thalamo-cortical (CSTC) circuits increases the spectral power of beta oscillations and results in Parkinson's disease motor symptoms. Analogous changes in parallel cognitive CSTC circuits involving the caudate and dorsolateral prefrontal cortex (DLPFC) may contribute to Parkinson's disease cognitive impairment. The objective of our study is to evaluate whether changes in beta oscillations in the caudate and DLPFC contribute to cognitive impairment in Parkinson's disease patients. To investigate this, we used local field potential recordings during deep brain stimulation surgery in 15 patients with Parkinson's disease. Local field potentials were recorded from DLPFC and caudate at rest and during a working memory task. We examined changes in beta oscillatory power during the working memory task as well as the relationship of beta oscillatory activity to preoperative cognitive status, as determined from neuropsychological testing results. We additionally conducted exploratory analyses on the relationship between cognitive impairment and task-based changes in spectral power in additional frequency bands. Spectral power of beta oscillations decreased in both DLPFC and caudate during working memory encoding and increased in these structures during feedback. Subjects with cognitive impairment had smaller decreases in caudate and DLPFC beta oscillatory power during encoding. In our exploratory analysis, we found that similar differences occurred in alpha frequencies in caudate and theta and alpha in DLPFC. Our findings suggest that oscillatory power changes in cognitive CSTC circuits may contribute to cognitive symptoms in patients with Parkinson's disease. These findings may inform the future development of novel neuromodulatory treatments for cognitive impairment in Parkinson's disease. [ABSTRACT FROM AUTHOR]

Executive functions, including working memory, are typically assessed clinically with neuropsychological instruments. In contrast, computerized tasks are used to test these cognitive functions in laboratory human and animal studies. Little is known of how neural activity captured by laboratory tasks relates to ability measured by clinical instruments and, by extension, clinical diagnoses of pathological conditions. We therefore sought to determine what aspects of neural activity elicited in laboratory tasks are predictive of performance in neuropsychological instruments. We recorded neural activity from intracranial electrodes implanted in human epilepsy patients as they performed laboratory working memory tasks. These patients had completed neuropsychological instruments preoperatively, including the Weschler Adult Intelligent Scale and the Wisconsin Card Sorting test. Our results revealed that increased high-gamma (70-150 Hz) power in the prefrontal and parietal cortex after presentation of visual stimuli to be remembered was indicative of lower performance in the neuropsychological tasks. On the other hand, we observed a positive correlation between high-frequency power amplitude in the delay period of the laboratory tasks and neuropsychological performance. Our results demonstrate how neural activity around task events relates to executive function and may be associated with clinical diagnosis of specific cognitive deficits.

Background and Objectives: Deep brain stimulation (DBS) is an effective treatment for Parkinson's disease (PD) motor symptoms. DBS is also associated with postoperative cognitive change in some patients. Previous studies found associations between medial active electrode contacts and overall cognitive decline. Our current aim is to determine the relationship between active electrode contact location and domain-specific cognitive changes., Methods: A single-institution retrospective cohort study was conducted in patients with PD who underwent subthalamic nucleus (STN) DBS from August 05, 2010, to February 22, 2021, and received preoperative and postoperative neuropsychological testing. Standardized norm-referenced test z-scores were categorized into attention, executive function, language, verbal memory, and visuospatial domains. SD change scores were averaged to create domain-specific change scores. We identified anterior commissure/posterior commissure coordinates of active electrode contacts in atlas space. We evaluated differences in active electrode contact location between patients with a domain score decrease of at least 1 SD and less than 1 SD. We performed multiple variable linear regression controlling for age, sex, education, time from surgery to postoperative neuropsychological testing (follow-up duration), disease duration, preoperative unified Parkinson's disease rating scale off medication scores, and preoperative memory scores to determine the relationship between active electrode contact location and domain change., Results: A total of 83 patients (male: n = 60, 72.3%) were included with a mean age of 63.6 ± 8.3 years, median disease duration of 9.0 [6.0, 11.5] years, and median follow-up duration of 8.0 [7.0, 11.0] months. More superior active electrode contact location in the left STN (P = .002) and higher preoperative memory scores (P < .0001) were associated with worsening memory. Active electrode contact location was not associated with change in other domains., Conclusion: In patients with PD who underwent STN DBS, we found an association between superior active electrode contacts in the left STN and verbal memory decline. Our study increases understanding of factors associated with cognitive change after DBS and may help inform postoperative programming., (Copyright © Congress of Neurological Surgeons 2024. All rights reserved.)