Presenting Author

Tomas Gomez Jr.

Presentation Type

Oral Presentation

Discipline Track

Clinical Science

Abstract Type

Research/Clinical

Abstract

Background: Parkinson’s disease (PD) is a neurodegenerative condition that affects movement, cognition, gait, and significantly impacts one's quality of life. Studies have suggested that neurotoxin pre-exposure is related to PD pathology and progressive motor/non-motor deficits, though it remains unclear how neurotoxin exposure affects neuroplasticity. The present study aimed to examine neurotoxin–induced PD-associated neuroplasticity changes in relationship to mental acuity and PD motor functionalities.

Methods: 7 voluntary participants experiencing early-stage PD symptoms with self-reported neurotoxin pre-exposure were enrolled in the longitudinal, repeated-measures clinical study; 2 sex-matched, age-matched, and occupation-matched healthy subjects were recruited for controlled comparative analysis (n=9). UTRGV’s Institute of Neuroscience (HION) served as study host, and its’ facilities aided in data capture for both sessions, baseline and post-2 months. During the baseline session participants self-disclosed neurotoxin pre-exposure (e.g. pesticides, Agent Orange, heavy metals, insecticides). Study staff then collected outcomes related to mental acuity (SLUMS), PD-associated gait abnormalities (HY Scale), non-motor/motor experiences burdening daily life (MDS-UPDRS), and arm motor functionalities. Corticospinal excitability and neuroplasticity were evaluated using Transcranial Magnetic Stimulation (TMS) in both groups. Specifically, we applied TMS at varying intensities to the area of the brain dedicated to the first dorsal interosseus (FDI) to evaluate neuroplasticity. Motor evoked potentials (MEPs) were recorded from the FDI at each assessed TMS intensity.

Results: Multivariate Analysis of Covariance revealed statistically significant mean differences in %MEP for Amplitude MEP and Area MEP after controlling for age, gender, mental status, HY ratings, motor function, and pre-stimuli EMG activity, [Pillai’s Trace = 0.24, F(18, 1358) =10.6, partial eta2 = 12%, p < .001]. Post-hoc ANOVA’s resulted statistically significant % MEP mean differences for EMG Area MEP, [F(9, 676) =18.0, partial eta2 = 19%, p < .001], and for EMG Amplitude MEP, F(9, 676) =19.0, partial eta2 = 20%, p < .001. HY ratings alone did not reveal statistical differences in mean EMG amplitude, p > .05, however, mean EMG Amplitude for % MEP 70-180 statistically fit a sigmoid model curve, F(1, 681) = 651.2, p < .001. The sigmoid model follows the specified equation, .

Conclusions: Our findings suggest potential clinical implications in PD conditions related to motor function, with specific relationships between HY ratings and sigmoid model insights into physiologically observed differences. Identified differences in Amplitude MEP and Area MEP highlight the importance of multivariate approaches to understanding MEP. Application of the present study can improve a variety of areas: e.g., physical therapy, neurotoxin regulation, even PD treatment. It can be speculated that variables such as age, gender, mental status, and pre-stimuli EMG activity should be carefully considered in future research on %MEP. Researchers should explore underlying mechanisms behind observed effects, interactions between variables, and clinical relevance of these findings. Specific implications may vary depending on the context of future research, e.g. characteristics of investigated populations, field of research (e.g., neurology, motor control, clinical rehabilitation), but nevertheless researchers should consider these conclusions in the broader context of existing literature and specific goals of investigation.

Academic/Professional Position

Undergraduate

Academic/Professional Position (Other)

Undergraduate Student Researcher

Mentor/PI Department

Neuroscience

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Exploring Neuroplasticity Changes in Neurotoxin-induced Parkinson’s Disease: A Preliminary Analysis using Transcranial Magnetic Stimulation

Background: Parkinson’s disease (PD) is a neurodegenerative condition that affects movement, cognition, gait, and significantly impacts one's quality of life. Studies have suggested that neurotoxin pre-exposure is related to PD pathology and progressive motor/non-motor deficits, though it remains unclear how neurotoxin exposure affects neuroplasticity. The present study aimed to examine neurotoxin–induced PD-associated neuroplasticity changes in relationship to mental acuity and PD motor functionalities.

Methods: 7 voluntary participants experiencing early-stage PD symptoms with self-reported neurotoxin pre-exposure were enrolled in the longitudinal, repeated-measures clinical study; 2 sex-matched, age-matched, and occupation-matched healthy subjects were recruited for controlled comparative analysis (n=9). UTRGV’s Institute of Neuroscience (HION) served as study host, and its’ facilities aided in data capture for both sessions, baseline and post-2 months. During the baseline session participants self-disclosed neurotoxin pre-exposure (e.g. pesticides, Agent Orange, heavy metals, insecticides). Study staff then collected outcomes related to mental acuity (SLUMS), PD-associated gait abnormalities (HY Scale), non-motor/motor experiences burdening daily life (MDS-UPDRS), and arm motor functionalities. Corticospinal excitability and neuroplasticity were evaluated using Transcranial Magnetic Stimulation (TMS) in both groups. Specifically, we applied TMS at varying intensities to the area of the brain dedicated to the first dorsal interosseus (FDI) to evaluate neuroplasticity. Motor evoked potentials (MEPs) were recorded from the FDI at each assessed TMS intensity.

Results: Multivariate Analysis of Covariance revealed statistically significant mean differences in %MEP for Amplitude MEP and Area MEP after controlling for age, gender, mental status, HY ratings, motor function, and pre-stimuli EMG activity, [Pillai’s Trace = 0.24, F(18, 1358) =10.6, partial eta2 = 12%, p < .001]. Post-hoc ANOVA’s resulted statistically significant % MEP mean differences for EMG Area MEP, [F(9, 676) =18.0, partial eta2 = 19%, p < .001], and for EMG Amplitude MEP, F(9, 676) =19.0, partial eta2 = 20%, p < .001. HY ratings alone did not reveal statistical differences in mean EMG amplitude, p > .05, however, mean EMG Amplitude for % MEP 70-180 statistically fit a sigmoid model curve, F(1, 681) = 651.2, p < .001. The sigmoid model follows the specified equation, .

Conclusions: Our findings suggest potential clinical implications in PD conditions related to motor function, with specific relationships between HY ratings and sigmoid model insights into physiologically observed differences. Identified differences in Amplitude MEP and Area MEP highlight the importance of multivariate approaches to understanding MEP. Application of the present study can improve a variety of areas: e.g., physical therapy, neurotoxin regulation, even PD treatment. It can be speculated that variables such as age, gender, mental status, and pre-stimuli EMG activity should be carefully considered in future research on %MEP. Researchers should explore underlying mechanisms behind observed effects, interactions between variables, and clinical relevance of these findings. Specific implications may vary depending on the context of future research, e.g. characteristics of investigated populations, field of research (e.g., neurology, motor control, clinical rehabilitation), but nevertheless researchers should consider these conclusions in the broader context of existing literature and specific goals of investigation.

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