| Poster | Poster Session 06 Program Schedule
02/15/2024
04:00 pm - 05:15 pm
Room: Majestic Complex (Posters 61-120)
Poster Session 06: Aging | MCI | Neurodegenerative Disease - PART 2
Final Abstract #75
Processing Speed in Parkinson’s Disease Patients on and off Levodopa
Jennifer Miller, Northwell Health, Manhasset, United States
Daliah Ross, UCSD, San Diego, United States
Paul Mattis, Northwell Health, Manhasset, United States
Category: Movement and Movement Disorders
Keyword 1: Parkinson's disease
Keyword 2: cognitive functioning
Keyword 3: neuropsychological assessment
Objective:
Bradykinesia, or motor slowing, is a hallmark feature of Parkinson’s disease (PD) and linked to decreased dopamine. Cognitive impairment is present in approximately 40% of patients with PD. Although PD can impact several cognitive domains, speed of processing is one of the most prominent areas of cognitive deficit. Several etiologies have been suggested to explain this, but many conclude that that processing speed deficits in PD are related to lower striatal dopamine. Previous findings have shown mixed effects of levodopa on cognitive and motor speed in PD. Therefore, this study examined the effects of levodopa on analogous tasks of written and oral processing speed performance.
Participants and Methods:
A sample of 49 adults (M age = 62.39, SD = 8.44; %female = 28.6) diagnosed with PD according to the UK Brain Bank criteria for idiopathic PD completed clinical and neuropsychological evaluation when “on” and “off” levodopa medication. The oral and written trials of the Symbol Digit Modalities Test (SDMT) were used to examine processing speed. Repeated measures t-tests were used to examine whether SDMT performance differed ON and OFF levodopa. A clinically-validated change score of 4 raw points was used to identify participants as “responders” and “non-responders” to levodopa, and characteristics of these groups were explored using t-tests and Mann-Whitney U tests, as appropriate.
Results:
On a group level, participants’ SDMT performance on oral (OFF: M = 46.98, SD = 11.98; ON: M = 47.73, SD = 9.95) and written (OFF: M = 39.10, SD = 10.21; ON: M = 39.98, SD = 9.39) trials did not differ while “on” versus “off” levodopa medication (p > .05). The levodopa-related change in oral and written SDMT performance was moderately correlated (r = .69, p < .001). On the written trial, 18 people with PD (36.7%) improved by 4 or more points were deemed “responders,” and 31 people (63.3%) as “non-responders.” 16 people (32.7%) improved by 4 or more points on the oral trials and were deemed “responders,” and 33 (67.3%) were “non-responders.” Oral SDMT responders had lower overall cognition (based on the Dementia Rating Scale, U = 35.50, p = .03), lower written SDMT (t = 2.62, p = .01), and lower oral SDMT (t = 2.40, p = .02) performance at baseline compared to non-responders. Written SDMT responders differed from non-responders based only on having lower written SDMT performance (t = 2.55, p = .01). Neither written nor oral responders differed from non-responders in terms of age, sex, or PD motor severity (MDS-Unified Parkinson's Disease Rating Scale, part 3 score; p > .05).
Conclusions:
Contrary to theoretical models of processing speed in PD being linked to dopamine, there was not a robust universal change in processing speed in PD “on” versus “off” levodopa medication. We found only a subset of participants with PD responded to levodopa in terms of processing speed. Responders had lower overall cognition and SDMT performance compared to non-responders, suggesting that only people with lower processing speed and cognitive functioning benefit from levodopa in terms of processing speed. Future work may examine how processing speed relates to PD-related cognitive and motor network patterns.
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